Volume 12, Issue 2

Transcatheter tricuspid interventions: time to re-think guidelines?

Ana Paula Tagliari, Maurizio Taramasso,

https://doi.org/10.18632/aging.102805 pp 1037—1038

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Tagliari AP, Taramasso M, . Transcatheter tricuspid interventions: time to re-think guidelines?. . 12:1037-1038. https://doi.org/10.18632/aging.102805

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In the heart of cardiac stromal senescence

Victorine Douin-Echinard, Lise Lefevre, Angelo Parini,

https://doi.org/10.18632/aging.102806 pp 1039—1041

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Targeting mitochondria to stimulate hematopoiesis

Mukul Girotra, Olaia Naveiras, Nicola Vannini,

https://doi.org/10.18632/aging.102807 pp 1042—1043

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Epigenetic chaperoning of aging

Stefanie Müthel, Baris Tursun,

https://doi.org/10.18632/aging.102808 pp 1044—1046

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CeRNA regulatory network-based analysis to study the roles of noncoding RNAs in the pathogenesis of intrahepatic cholangiocellular carcinoma

Weiyu Xu, Si Yu, Jianping Xiong, Junyu Long, Yongchang Zheng, Xinting Sang,

https://doi.org/10.18632/aging.102634 pp 1047—1086

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Xu W, Yu S, Xiong J, Long J, Zheng Y, Sang X, . CeRNA regulatory network-based analysis to study the roles of noncoding RNAs in the pathogenesis of intrahepatic cholangiocellular carcinoma. . 12:1047-1086. https://doi.org/10.18632/aging.102634

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                TY  - JOUR
                AU  - Xu, Weiyu 
                AU  - Yu, Si 
                AU  - Xiong, Jianping 
                AU  - Long, Junyu 
                AU  - Zheng, Yongchang 
                AU  - Sang, Xinting 
                TI  - CeRNA regulatory network-based analysis to study the roles of noncoding RNAs in the pathogenesis of intrahepatic cholangiocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102634
                DO  - 10.18632/aging.102634
                SP  - 1047
                EP  - 1086
                PY  - 
                AB  - To explore and understand the competitive mechanism of ceRNAs in intrahepatic cholangiocarcinoma (ICC), we used bioinformatics analysis methods to construct an ICC-related ceRNA regulatory network (ceRNET), which contained 340 lncRNA-miRNA-mRNA regulatory relationships based on the RNA expression datasets in the NCBI GEO database. We identified the core regulatory pathway RP11-328K4.1-hsa-miR-27a-3p-PROS1, which is related to ICC, for further validation by molecular biology assays. GO analysis of 44 differentially expressed mRNAs in ceRNET revealed that they were mainly enriched in biological processes including &#x201C;negative regulation of epithelial cell proliferation&#x201D; and &quot;positive regulation of activated T lymphocyte proliferation.&#x201D; KEGG analysis showed that they were mainly enriched in the &#x201C;complement and coagulation cascade&#x201D; pathway. The molecular biology assay showed that lncRNA RP11-328K4.1 expression was significantly lower in the cancerous tissues and peripheral plasma of ICC patients than in normal controls (p&lt;0.05). In addition, hsa-miR-27a-3p was found to be significantly upregulated in the cancer tissues and peripheral plasma of ICC patients (p&lt;0.05). Compared to normal controls, the expression of PROS1 mRNA was significantly downregulated in ICC patient cancer tissues (p&lt;0.05) but not in peripheral plasma (p&gt;0.05). Furthermore, ROC analysis revealed that RP11-328K4.1, hsa-miR-27a-3p, and PROS1 had significant diagnostic value in ICC. We concluded that the upregulation of lncRNA RP11-328K4.1, which might act as a miRNA sponge, exerts an antitumor effect in ICC by eliminating the inhibition of PROS1 mRNA expression by oncogenic miRNA hsa-miR-27a.
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Metformin attenuates cartilage degeneration in an experimental osteoarthritis model by regulating AMPK/mTOR

Xiaofeng Feng, Jianying Pan, Junyan Li, Chun Zeng, Weizhong Qi, Yan Shao, Xin Liu, Liangliang Liu, Guozhi Xiao, Haiyan Zhang, Xiaochun Bai, Daozhang Cai,

https://doi.org/10.18632/aging.102635 pp 1087—1103

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Feng X, Pan J, Li J, Zeng C, Qi W, Shao Y, Liu X, Liu L, Xiao G, Zhang H, Bai X, Cai D, . Metformin attenuates cartilage degeneration in an experimental osteoarthritis model by regulating AMPK/mTOR. . 12:1087-1103. https://doi.org/10.18632/aging.102635

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                TY  - JOUR
                AU  - Feng, Xiaofeng 
                AU  - Pan, Jianying 
                AU  - Li, Junyan 
                AU  - Zeng, Chun 
                AU  - Qi, Weizhong 
                AU  - Shao, Yan 
                AU  - Liu, Xin 
                AU  - Liu, Liangliang 
                AU  - Xiao, Guozhi 
                AU  - Zhang, Haiyan 
                AU  - Bai, Xiaochun 
                AU  - Cai, Daozhang 
                TI  - Metformin attenuates cartilage degeneration in an experimental osteoarthritis model by regulating AMPK/mTOR
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102635
                DO  - 10.18632/aging.102635
                SP  - 1087
                EP  - 1103
                PY  - 
                AB  - Background: It is generally thought that the occurrence and progression of osteoarthritis (OA) results from multiple causes, including degradation and destruction of the cartilage matrix and aging of chondrocytes. Metformin is a first-line drug for the treatment of diabetes, and has great potential for the treatment of other disorders. However, the role of metformin in OA is unknown.Results: Metformin displayed a protective effect against OA. There were lower OARSI scores and fewer MMP-13-positive cells in DMM mice and cartilage explants after treatment with metformin. In addition, metformin treatment decreased p16INK4a levels in OA chondrocytes, and enhanced polarization of AMPK and inhibition of mTORC1 in OA mice and chondrocytes in a dose-dependent manner.Conclusions: Metformin effectively alleviated cartilage degradation and aging through regulation of the AMPK/mTOR signaling pathways, suggesting that it could be an effective treatment for OA.Methods: The effects of metformin on cartilage degradation and chondrocyte aging was determined in a destabilization of the medial meniscus (DMM)-induced OA mouse model and in IL-1&#x3B2;-treated mouse chondrocytes and cartilage explants. Articular cartilage degeneration was graded using the Osteoarthritis Research Society International (OARSI) criteria. Immunostaining, RT-PCR, and western blot analyses were conducted to detect the relative expressions of protein and RNA.
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Body mass index and albumin levels are prognostic factors for long-term survival in elders with limited performance status

Kuan-Yu Lai, Tai-Hsien Wu, Chiu-Shong Liu, Chih-Hsueh Lin, Cheng-Chieh Lin, Ming-May Lai, Wen-Yuan Lin,

https://doi.org/10.18632/aging.102642 pp 1104—1113

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Lai K, Wu T, Liu C, Lin C, Lin C, Lai M, Lin W, . Body mass index and albumin levels are prognostic factors for long-term survival in elders with limited performance status. . 12:1104-1113. https://doi.org/10.18632/aging.102642

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                TY  - JOUR
                AU  - Lai, Kuan-Yu 
                AU  - Wu, Tai-Hsien 
                AU  - Liu, Chiu-Shong 
                AU  - Lin, Chih-Hsueh 
                AU  - Lin, Cheng-Chieh 
                AU  - Lai, Ming-May 
                AU  - Lin, Wen-Yuan 
                TI  - Body mass index and albumin levels are prognostic factors for long-term survival in elders with limited performance status
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102642
                DO  - 10.18632/aging.102642
                SP  - 1104
                EP  - 1113
                PY  - 
                AB  - Elderly long-term care facility residents typically have musculoskeletal conditions that may lead to long-term disability and increased mortality. Our main objective was to explore the relationship between body mass index (BMI), albumin levels, and mortality in elderly individuals with limited performance status. Among 182 participants (mean age, 78.8 years; 57% women), 11%, 64%, and 25% had serum albumin levels of &lt;2.8, 2.8-3.5, and &gt;3.5 g/dL, respectively. After multivariate adjustments, diastolic blood pressure &gt;90 mmHg was associated with all-cause mortality [hazard ratio (HR) = 2.08, 95% confidence interval (CI) = 1.13-3.82; P = 0.018]. In addition, BMI &lt;18.5 kg/m2 and albumin level &lt;2.8 g/dL associated with higher mortality than BMI = 18.5-24 kg/m2 and albumin level &gt; 3.5 g/dL (HR = 1.80, 95% CI = 1.11-2.94 and HR = 2.54, 95% CI 1.22-5.30, respectively; P = 0.018 and 0.013, respectively). Highest mortality was noted in participants with albumin levels &lt;2.8 g/dL and BMIs &lt;18.5 kg/m2 (HR = 6.12, 95% CI = 1.85-20.21, P = 0.003). Combined hypoalbuminemia (albumin level &lt; 2.8 g/dL) and low BMI (&lt;18.5 kg/m2) may be a useful prognostic indicator of high mortality risk in elderly individuals with limited performance status.
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Romo1 is involved in the immune response of glioblastoma by regulating the function of macrophages

Guan Sun, Ying Cao, Chunfa Qian, Zhengqiang Wan, Jian Zhu, Jun Guo, Lei Shi,

https://doi.org/10.18632/aging.102648 pp 1114—1127

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Sun G, Cao Y, Qian C, Wan Z, Zhu J, Guo J, Shi L, . Romo1 is involved in the immune response of glioblastoma by regulating the function of macrophages. . 12:1114-1127. https://doi.org/10.18632/aging.102648

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                TY  - JOUR
                AU  - Sun, Guan 
                AU  - Cao, Ying 
                AU  - Qian, Chunfa 
                AU  - Wan, Zhengqiang 
                AU  - Zhu, Jian 
                AU  - Guo, Jun 
                AU  - Shi, Lei 
                TI  - Romo1 is involved in the immune response of glioblastoma by regulating the function of macrophages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102648
                DO  - 10.18632/aging.102648
                SP  - 1114
                EP  - 1127
                PY  - 
                AB  - Reactive oxygen species (ROS) modulator 1 (Romo1) is a mitochondrial membrane protein that is essential for the regulation of mitochondrial ROS production and redox sensing. Although the physiological functions of Romo1 have been studied for the past few years, the role of Romo1 in cancer remained unclear. In this study, we found that the high expression of Romo1 is associated with the poor prognosis of glioblastoma patients. Further study revealed that Romo1 is highly expressed in macrophages, indicating that the overexpression of Romo1 may participate in the function of macrophages and contribute to the progression of glioblastoma. Through the glioblastoma mouse model, we found that the overexpression of Romo1 in bone marrow cells significantly inhibited the immune response within tumor microenvironment, and that the overexpression of Romo1 resulted in the M2 polarization of bone marrow derived macrophages (BMDMs) through mTORC1 signaling pathway. In addition, the inhibition of Romo1 combining with anti-PD-1 immunotherapy significantly improved the survival outcome of glioblastoma in mouse model. Collectively, our study highlights the important role of Romo1 in immune response especially the function of macrophages, and implicates it as a potential target of immunotherapy for glioblastoma.
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Development of frailty subtypes and their associated risk factors among the community-dwelling elderly population

Yan Zhang, Xiu-Juan Xu, Ting-Yu Lian, Ling-Feng Huang, Jin-Mei Zeng, Dong-Mei Liang, Ming-Juan Yin, Jing-Xiao Huang, Liang-Chang Xiu, Zu-Wei Yu, Yu-Lian Li, Chen Mao, Jin-Dong Ni,

https://doi.org/10.18632/aging.102671 pp 1128—1140

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Zhang Y, Xu X, Lian T, Huang L, Zeng J, Liang D, Yin M, Huang J, Xiu L, Yu Z, Li Y, Mao C, Ni J, . Development of frailty subtypes and their associated risk factors among the community-dwelling elderly population. . 12:1128-1140. https://doi.org/10.18632/aging.102671

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                TY  - JOUR
                AU  - Zhang, Yan 
                AU  - Xu, Xiu-Juan 
                AU  - Lian, Ting-Yu 
                AU  - Huang, Ling-Feng 
                AU  - Zeng, Jin-Mei 
                AU  - Liang, Dong-Mei 
                AU  - Yin, Ming-Juan 
                AU  - Huang, Jing-Xiao 
                AU  - Xiu, Liang-Chang 
                AU  - Yu, Zu-Wei 
                AU  - Li, Yu-Lian 
                AU  - Mao, Chen 
                AU  - Ni, Jin-Dong 
                TI  - Development of frailty subtypes and their associated risk factors among the community-dwelling elderly population
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102671
                DO  - 10.18632/aging.102671
                SP  - 1128
                EP  - 1140
                PY  - 
                AB  - In order to explore frailty subtypes and find their associated risk factors, we conducted cross-sectional surveys of 5,341 seniors aged 60 and over in China using the Frailty Index (FI) scale. We identified four frailty subtypes, namely multi-frail, cognitive and functionally frail, psychologically frail and physiologically frail. Old age and low education level were the common risk factors among the four subtypes. Being widowed, divorced or unmarried was a risk factor for multi-frail, cognitive and functionally frail and psychologically frail, and male sex was a protective factor against cognitive and functionally frail and psychologically frail subtypes. Having a harmonious relationship with family was a protective factor against multi-frail, and fewer visits to the elderly by their children was a risk factor for psychologically frail. Dissatisfaction with their housing was a risk factor for cognitive and functionally frail, psychologically frail and physiologically frail, and a pension being the main source of income was a risk factor for cognitive and functionally frail and psychologically frail. Exercising every day was a protective factor against multi-frail and cognitive and functionally frail, and a lower level of physical activity was a risk factor for all four frailty subtypes. Our findings confirm the heterogeneity of frailty and suggest that different frail elderly individuals need more targeted care interventions.
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MiR-29b-3p promotes particulate matter-induced inflammatory responses by regulating the C1QTNF6/AMPK pathway

Jian Wang, Mengchan Zhu, Ling Ye, Cuicui Chen, Jun She, Yuanlin Song,

https://doi.org/10.18632/aging.102672 pp 1141—1158

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Wang J, Zhu M, Ye L, Chen C, She J, Song Y, . MiR-29b-3p promotes particulate matter-induced inflammatory responses by regulating the C1QTNF6/AMPK pathway. . 12:1141-1158. https://doi.org/10.18632/aging.102672

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                TY  - JOUR
                AU  - Wang, Jian 
                AU  - Zhu, Mengchan 
                AU  - Ye, Ling 
                AU  - Chen, Cuicui 
                AU  - She, Jun 
                AU  - Song, Yuanlin 
                TI  - MiR-29b-3p promotes particulate matter-induced inflammatory responses by regulating the C1QTNF6/AMPK pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102672
                DO  - 10.18632/aging.102672
                SP  - 1141
                EP  - 1158
                PY  - 
                AB  - Inflammatory responses are considered to be the critical mechanism underlying particulate matter (PM)-induced development and exacerbation of chronic respiratory diseases. MiR-29b-3p has been found to participate in various biological processes, but its role in PM-induced inflammatory responses was previously unknown. Here, we constructed a miRNA PCR array to find that miR-29b-3p was the most highly expressed in human bronchial epithelial cells (HBECs) exposed to PM. MiR-29b-3p promoted PM-induced pro-inflammatory cytokines (IL-1&#x3B2;, IL-6, and IL-8) expression via inhibiting the AMPK signaling pathway in HBECs. RNA sequencing and luciferase reporter assay identified that miR-29b-3p targeted complement C1q tumor necrosis factor-related protein 6 (C1QTNF6), a protein that protected from PM-induced inflammatory responses via activating the AMPK signaling pathway. In vivo, miR-29b-3p antagomirs delivered via the tail vein prior to PM exposure significantly counteracted PM-induced miR-29b-3p upregulation and C1QTNF6 downregulation in lung tissues. Furthermore, miR-29b-3p inhibition alleviated inflammatory cells infiltration and pro-inflammatory cytokines secretion in the lung of PM-exposed mice. These findings firstly revealed that miR-29b-3p acted as a novel modulator of PM-induced inflammatory responses by targeting the C1QTNF6/AMPK signaling pathway, which contributes to a better understanding of the biological mechanisms underlying adverse PM-induced respiratory health effects.
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Circular RNA HIPK3 downregulation mediates hydrogen peroxide-induced cytotoxicity in human osteoblasts

Jinqian Liang, Ying-chao Shen, Xiang-yang Zhang, Chong Chen, Hong Zhao, Jianhua Hu,

https://doi.org/10.18632/aging.102674 pp 1159—1170

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Liang J, Shen Y, Zhang X, Chen C, Zhao H, Hu J, . Circular RNA HIPK3 downregulation mediates hydrogen peroxide-induced cytotoxicity in human osteoblasts. . 12:1159-1170. https://doi.org/10.18632/aging.102674

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                TY  - JOUR
                AU  - Liang, Jinqian 
                AU  - Shen, Ying-chao 
                AU  - Zhang, Xiang-yang 
                AU  - Chen, Chong 
                AU  - Zhao, Hong 
                AU  - Hu, Jianhua 
                TI  - Circular RNA HIPK3 downregulation mediates hydrogen peroxide-induced cytotoxicity in human osteoblasts
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102674
                DO  - 10.18632/aging.102674
                SP  - 1159
                EP  - 1170
                PY  - 
                AB  - Hydrogen peroxide (H2O2) induces oxidative injury to human osteoblasts. The expression and potential function of circular RNA HIPK3 (circHIPK3) in H2O2-treated human osteoblasts were tested. We show that H2O2 significantly downregulated circHIPK3 in OB-6 cells and primary human osteoblasts. Furthermore, circHIPK3 levels were decreased in the necrotic femoral head tissues of dexamethasone-treated patients. In OB-6 osteoblastic cells and primary human osteoblasts, forced overexpression of circHIPK3 by a lentiviral construct alleviated H2O2-induced viability reduction, cell death and apoptosis. Contrarily, circHIPK3 silencing by targeted shRNA potentiated H2O2-induced cytotoxicity in OB-6 cells and primary human osteoblasts. Moreover, circHIPK3 downregulation by H2O2 induced miR-124 accumulation in OB-6 cells and primary human osteoblasts. On the contrary, miR-124 inhibition by transfection of the miR-124 inhibitor protected human osteoblasts from H2O2. Importantly, forced overexpression of miR-124 by transfection of the miR-124 mimic induced significant cytotoxicity in OB-6 cells and primary human osteoblasts. H2O2 downregulated miR-124&#x2019;s targets, cyclin dependent kinase 6 and Rho-Associated Protein Kinase 1, in human osteoblasts. In conclusion circHIPK3 downregulation mediates H2O2-induced cytotoxicity in human osteoblasts.
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DNASE1L3 as an indicator of favorable survival in hepatocellular carcinoma patients following resection

Shuncong Wang, Haiqing Ma, Xuemin Li, Xiangqiong Mo, Haiyu Zhang, Lewei Yang, Yun Deng, Yan Yan, Guangwei Yang, Xingwei Liu, Huanhuan Sun,

https://doi.org/10.18632/aging.102675 pp 1171—1185

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Wang S, Ma H, Li X, Mo X, Zhang H, Yang L, Deng Y, Yan Y, Yang G, Liu X, Sun H, . DNASE1L3 as an indicator of favorable survival in hepatocellular carcinoma patients following resection. . 12:1171-1185. https://doi.org/10.18632/aging.102675

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                TY  - JOUR
                AU  - Wang, Shuncong 
                AU  - Ma, Haiqing 
                AU  - Li, Xuemin 
                AU  - Mo, Xiangqiong 
                AU  - Zhang, Haiyu 
                AU  - Yang, Lewei 
                AU  - Deng, Yun 
                AU  - Yan, Yan 
                AU  - Yang, Guangwei 
                AU  - Liu, Xingwei 
                AU  - Sun, Huanhuan 
                TI  - DNASE1L3 as an indicator of favorable survival in hepatocellular carcinoma patients following resection
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102675
                DO  - 10.18632/aging.102675
                SP  - 1171
                EP  - 1185
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is a common malignancy with a dismal prognosis. It is of great importance to identify biomarkers for the prediction of patients&#x2019; survival.The mRNA expression level of deoxyribonuclease 1 like 3 (DNASE1L3) and its correlation with survival were accessed in 424 samples from The Cancer Genome Atlas database. Its expression level was confirmed by real-time quantitative polymerase chain reaction and western blotting in 20 pairs of postsurgical specimens. In addition, immunohistochemistry staining of DNASE1L3 was also performed in 113 postoperative samples, using a histochemistry score system. The relationship between patients&#x2019; survival and DNASE1L3 expression level was evaluated by the Kaplan-Meier method.DNASE1L3 is downregulated in both mRNA and protein levels in HCC tissues, compared with adjacent normal tissues. 52 of 113 HCC specimens showed positive DNASE1L3 protein expression. Patients with positive DNASE1L3 expression had significantly longer overall survival, compared with patients with negative expression (p = 0.023). However, the DNASE1L3 fails to discriminate progression-free survival (p = 0.134). Multivariate COX analysis revealed that positive DNASE1L3 expression and higher differentiation were significantly associated with better overall survival.This study demonstrated that positive DNASE1L3 expression is an independent prognostic factor for better survival in HCC patients following radical resection.
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Fibroblast growth factor 10 alleviates particulate matter-induced lung injury by inhibiting the HMGB1-TLR4 pathway

Lingjing Liu, Chenjian Song, Jingli Li, Qiang Wang, Mingyang Zhu, Yiran Hu, Junjie Chen, Chaolei Chen, Jin-San Zhang, Nian Dong, Chengshui Chen,

https://doi.org/10.18632/aging.102676 pp 1186—1200

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Liu L, Song C, Li J, Wang Q, Zhu M, Hu Y, Chen J, Chen C, Zhang J, Dong N, Chen C, . Fibroblast growth factor 10 alleviates particulate matter-induced lung injury by inhibiting the HMGB1-TLR4 pathway. . 12:1186-1200. https://doi.org/10.18632/aging.102676

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                TY  - JOUR
                AU  - Liu, Lingjing 
                AU  - Song, Chenjian 
                AU  - Li, Jingli 
                AU  - Wang, Qiang 
                AU  - Zhu, Mingyang 
                AU  - Hu, Yiran 
                AU  - Chen, Junjie 
                AU  - Chen, Chaolei 
                AU  - Zhang, Jin-San 
                AU  - Dong, Nian 
                AU  - Chen, Chengshui 
                TI  - Fibroblast growth factor 10 alleviates particulate matter-induced lung injury by inhibiting the HMGB1-TLR4 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102676
                DO  - 10.18632/aging.102676
                SP  - 1186
                EP  - 1200
                PY  - 
                AB  - Exposure to particulate matter (PM) is associated with increased incidence of respiratory diseases. The present study aimed to investigate the roles of fibroblast growth factor 10 (FGF10) in PM-induced lung injury. Mice were intratracheally instilled with FGF10 or phosphate-buffered saline at one hour before instillation of PM for two consecutive days. In addition, the anti-inflammatory impact of FGF10 in vitro and its effect on the high-mobility group box 1 (HMGB1)-toll-like receptor 4 (TLR4) pathway was investigated. It was found that PM exposure is associated with increased inflammatory cell infiltration into the lung and increased vascular protein leakage, while FGF10 pretreatment attenuated both of these effects. FGF10 also decreased the PM-induced expression of interleukin (IL)-6, IL-8, tumor necrosis factor-&#x3B1; and HMGB1 in murine bronchoalveolar lavage fluid and in the supernatants of human bronchial epithelial cells exposed to PM. FGF10 exerted anti-inflammatory and cytoprotective effects by inhibiting the HMGB1-TLR4 pathway. These results indicate that FGF10 may have therapeutic values for PM-induced lung injury.
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Increased serum salusin-α by aerobic exercise training correlates with improvements in arterial stiffness in middle-aged and older adults

Shumpei Fujie, Natsuki Hasegawa, Kiyoshi Sanada, Takafumi Hamaoka, Seiji Maeda, Jaume Padilla, Luis A. Martinez-Lemus, Motoyuki Iemitsu,

https://doi.org/10.18632/aging.102678 pp 1201—1212

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Fujie S, Hasegawa N, Sanada K, Hamaoka T, Maeda S, Padilla J, Martinez-Lemus LA, Iemitsu M, . Increased serum salusin-α by aerobic exercise training correlates with improvements in arterial stiffness in middle-aged and older adults. . 12:1201-1212. https://doi.org/10.18632/aging.102678

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                TY  - JOUR
                AU  - Fujie, Shumpei 
                AU  - Hasegawa, Natsuki 
                AU  - Sanada, Kiyoshi 
                AU  - Hamaoka, Takafumi 
                AU  - Maeda, Seiji 
                AU  - Padilla, Jaume 
                AU  - Martinez-Lemus, Luis A. 
                AU  - Iemitsu, Motoyuki 
                TI  - Increased serum salusin-α by aerobic exercise training correlates with improvements in arterial stiffness in middle-aged and older adults
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102678
                DO  - 10.18632/aging.102678
                SP  - 1201
                EP  - 1212
                PY  - 
                AB  - Aging causes arterial stiffening which can be mitigated by increased physical activity. Although low circulating levels of salusin-&#x3B1; are associated with cardiovascular disease, whether salusin-&#x3B1; decreases with aging and whether the reduced arterial stiffening occurring with exercise training is associated with increased serum salusin-&#x3B1; is unknown. Herein we assessed carotid-femoral pulse wave velocity (cfPWV), systolic (SBP) and diastolic (DBP) blood pressures in a cross-sectional study that compared young (20-39-year-old, n=45) versus middle-aged and older (40-80-year-old, n=60) subjects. We also performed an interventional study in which 36 young and 40 middle-aged and older subjects underwent eight weeks of aerobic exercise training. In the cross-sectional study, serum salusin-&#x3B1; levels were lesser in middle-aged and older subjects compared to young individuals and negatively correlated with age, SBP, DBP, or cfPWV. In the interventional study, exercise training increased serum salusin-&#x3B1; in middle-aged and older subjects. Notably, negative correlations were noted between the exercise training-induced changes in serum salusin-&#x3B1; and cfPWV, SBP and DBP. Results indicate that advanced age associates with low circulating salusin-&#x3B1;, the levels of which can be augmented by exercise training. Importantly, increased serum salusin-&#x3B1; with exercise correlates with improvements in arterial stiffness and a reduction in blood pressure.
                ER  -

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MicroRNA-200a induces immunosuppression by promoting PTEN-mediated PD-L1 upregulation in osteosarcoma

Zhuochao Liu, Junxiang Wen, Chuanlong Wu, Chuanzhen Hu, Jun Wang, Qiyuan Bao, Hongyi Wang, Jizhuang Wang, Qi Zhou, Li Wei, Yuhui Shen, Weibin Zhang,

https://doi.org/10.18632/aging.102679 pp 1213—1236

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Liu Z, Wen J, Wu C, Hu C, Wang J, Bao Q, Wang H, Wang J, Zhou Q, Wei L, Shen Y, Zhang W, . MicroRNA-200a induces immunosuppression by promoting PTEN-mediated PD-L1 upregulation in osteosarcoma. . 12:1213-1236. https://doi.org/10.18632/aging.102679

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                TY  - JOUR
                AU  - Liu, Zhuochao 
                AU  - Wen, Junxiang 
                AU  - Wu, Chuanlong 
                AU  - Hu, Chuanzhen 
                AU  - Wang, Jun 
                AU  - Bao, Qiyuan 
                AU  - Wang, Hongyi 
                AU  - Wang, Jizhuang 
                AU  - Zhou, Qi 
                AU  - Wei, Li 
                AU  - Shen, Yuhui 
                AU  - Zhang, Weibin 
                TI  - MicroRNA-200a induces immunosuppression by promoting PTEN-mediated PD-L1 upregulation in osteosarcoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102679
                DO  - 10.18632/aging.102679
                SP  - 1213
                EP  - 1236
                PY  - 
                AB  - In this study, we identified microRNAs that regulate the expression of programmed death-ligand 1(PD-L1) in osteosarcoma and investigated their role in PD-L1-targeted immunotherapy. MicroRNA sequencing analysis showed that the expression of PD-L1 is regulated by microRNA-200a in U2OS, 143B, and K7 osteosarcoma cells. MicroRNA-200a overexpression induced the upregulation of PD-L1 in the osteosarcoma cells. CD8+ T cells co-cultured with microRNA-200a-overexpressing osteosarcoma cells showed reduced survival, proliferation, and secretion of granzyme B and perforin. The same phenomenon was also observed in the K7-derived syngeneic mouse model, as microRNA-200a promoted tumor growth by increasing the percentage of Foxp3+ regulatory T lymphocytes while reducing the proportions of CD4+, CD8+, and IFN-&#x3B3;+ cytotoxic T lymphocytes. But microRNA-200a overexpression group was also more responsive to PD-L1-targeted immunotherapy than the controls. In addition, the tumor tissues from 32 osteosarcoma patients showed that high expression of microRNA-200a and PD-L1 was associated with poor tumor necrosis rate after chemotherapy. Moreover, we confirmed that tensin homolog deleted on chromosome ten (PTEN) could act as the target gene for microRNA-200a during the upregulation of PD-L1. Thus, our findings provide important and novel insight into a regulatory axis involving microRNA-200a/PTEN/ PD-L1 axis, which determines osteosarcoma growth and the efficacy of PD-L1-targeted immunotherapy.
                ER  -

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AR-induced ZEB1-AS1 represents poor prognosis in cholangiocarcinoma and facilitates tumor stemness, proliferation and invasion through mediating miR-133b/HOXB8

Xingming Jiang, Jinglin Li, Weina Wang, Zengtao Hu, Canghai Guan, Yuqiao Zhao, Wenzhi Li, Yunfu Cui,

https://doi.org/10.18632/aging.102680 pp 1237—1255

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Jiang X, Li J, Wang W, Hu Z, Guan C, Zhao Y, Li W, Cui Y, . AR-induced ZEB1-AS1 represents poor prognosis in cholangiocarcinoma and facilitates tumor stemness, proliferation and invasion through mediating miR-133b/HOXB8. . 12:1237-1255. https://doi.org/10.18632/aging.102680

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                TY  - JOUR
                AU  - Jiang, Xingming 
                AU  - Li, Jinglin 
                AU  - Wang, Weina 
                AU  - Hu, Zengtao 
                AU  - Guan, Canghai 
                AU  - Zhao, Yuqiao 
                AU  - Li, Wenzhi 
                AU  - Cui, Yunfu 
                TI  - AR-induced ZEB1-AS1 represents poor prognosis in cholangiocarcinoma and facilitates tumor stemness, proliferation and invasion through mediating miR-133b/HOXB8
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102680
                DO  - 10.18632/aging.102680
                SP  - 1237
                EP  - 1255
                PY  - 
                AB  - Zinc finger E-box binding homeobox 1 antisense 1 (ZEB1-AS1) has displayed vital regulatory function in various tumors. However, the biological function of ZEB1-AS1 in cholangiocarcinoma (CCA) remains unclear. In this study, we confirmed that ZEB1-AS1 expression was increased in CCA tissues and cells, respectively. Upregulated ZEB1-AS1 was related to lymph node invasion, advanced TNM stage and poor survival of CCA patients. ZEB1-AS1 exhibited high sensitivity and specificity to be an independent poor prognostic factor of patients with CCA. Functionally, knocking down ZEB1-AS1 attenuated tumor cell stemness, restrained cellular viability in vitro and in vivo, and inhibited CCA cell migration and invasion by reversing epithelial-mesenchymal transition. For the mechanism, androgen receptor (AR) directly promoted ZEB1-AS1 expression, and further ZEB1-AS1 increased oncogene homeobox B8 (HOXB8) by sponging miR-133b. In addition, malignant phenotypes of CCA promoted by ZEB1-AS1 dysregulation were rescued separately through interfering miR-133b and HOXB8, suggesting AR/ZEB1-AS1/miR-133b/HOXB8 exerted crucial functions in tumorigenesis and progression of CCA.
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Ubiquinol-10 delays postovulatory oocyte aging by improving mitochondrial renewal in pigs

Ying-Jie Niu, Wenjun Zhou, Zheng-Wen Nie, Dongjie Zhou, Yong-Nan Xu, Sun A. Ock, Chang-Guo Yan, Xiang-Shun Cui,

https://doi.org/10.18632/aging.102681 pp 1256—1271

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Niu Y, Zhou W, Nie Z, Zhou D, Xu Y, Ock SA, Yan C, Cui X, . Ubiquinol-10 delays postovulatory oocyte aging by improving mitochondrial renewal in pigs. . 12:1256-1271. https://doi.org/10.18632/aging.102681

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                TY  - JOUR
                AU  - Niu, Ying-Jie 
                AU  - Zhou, Wenjun 
                AU  - Nie, Zheng-Wen 
                AU  - Zhou, Dongjie 
                AU  - Xu, Yong-Nan 
                AU  - Ock, Sun A. 
                AU  - Yan, Chang-Guo 
                AU  - Cui, Xiang-Shun 
                TI  - Ubiquinol-10 delays postovulatory oocyte aging by improving mitochondrial renewal in pigs
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102681
                DO  - 10.18632/aging.102681
                SP  - 1256
                EP  - 1271
                PY  - 
                AB  - Ubiquinol-10, the reduced form of coenzyme Q10, protects mammalian cells from oxidative damage and enhances mitochondrial activity. However, the protective effect of ubiquinol-10 on mammalian oocytes is not well understood. In this study, we investigated the effect of ubiquinol-10 on porcine oocytes during postovulatory aging. Metaphase II oocytes were selected as fresh oocytes and further cultured for 48 h with different concentrations of ubiquinol-10 (0&#x2013;400 &#x3BC;M) in vitro as a postovulatory aging model. After choosing the optimal concentration of ubiquinol-10 (100 &#x3BC;M) that maintained oocyte morphology and developmental competence during the progression of aging, the oocytes were randomly divided into five groups: fresh, control-24 h, ubiquinol-24 h, control-48 h, and ubiquinol-48 h. The results revealed that ubiquinol-10 significantly prevented aging-induced oxidative stress, GSH reduction, cytoskeleton impairment, apoptosis, and autophagy. Mitochondrial biogenesis (SIRT1 and PGC-1&#x3B1;) and mitophagy (PINK1 and PARKIN)-related proteins were decreased during aging. Addition of ubiquinol-10 prevented the aging-induced reduction of these proteins. Consequently, although mitochondrial content was decreased, the number of active mitochondria and ATP level were significantly increased upon treatment with ubiquinol-10. Thus, ubiquinol-10 has beneficial effects on porcine postovulatory aging oocytes owing to its antioxidant properties and ability to promote mitochondrial renewal.
                ER  -

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FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice

Chi Zhang, Yun Xie, Haicheng Chen, Linyan Lv, Jiahui Yao, Min Zhang, Kai Xia, Xin Feng, Yanqing Li, Xiaoyan Liang, Xiangzhou Sun, Chunhua Deng, Guihua Liu,

https://doi.org/10.18632/aging.102682 pp 1272—1284

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Zhang C, Xie Y, Chen H, Lv L, Yao J, Zhang M, Xia K, Feng X, Li Y, Liang X, Sun X, Deng C, Liu G, . FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice. . 12:1272-1284. https://doi.org/10.18632/aging.102682

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                TY  - JOUR
                AU  - Zhang, Chi 
                AU  - Xie, Yun 
                AU  - Chen, Haicheng 
                AU  - Lv, Linyan 
                AU  - Yao, Jiahui 
                AU  - Zhang, Min 
                AU  - Xia, Kai 
                AU  - Feng, Xin 
                AU  - Li, Yanqing 
                AU  - Liang, Xiaoyan 
                AU  - Sun, Xiangzhou 
                AU  - Deng, Chunhua 
                AU  - Liu, Guihua 
                TI  - FOXO4-DRI alleviates age-related testosterone secretion insufficiency by targeting senescent Leydig cells in aged mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102682
                DO  - 10.18632/aging.102682
                SP  - 1272
                EP  - 1284
                PY  - 
                AB  - Male late-onset hypogonadism is an age-related disease, the core mechanism of which is dysfunction of senescent Leydig cells. Recent studies have shown that elimination of senescent cells can restore proper homeostasis to aging tissue. In the present study, we found that the fork head box O (FOXO) transcription factor FOXO4 was specially expressed in human Leydig cells and that its translocation to the nucleus in the elderly was related to decreased testosterone synthesis. Using hydrogen peroxide-induced senescent TM3 Leydig cells as an in vitro model, we observed that FOXO4 maintains the viability of senescent Leydig cells and suppresses their apoptosis. By disrupting the FOXO4-p53 interaction, FOXO4-DRI, a specific FOXO4 blocker, selectively induced p53 nuclear exclusion and apoptosis in senescent Leydig cells. In naturally aged mice, FOXO4-DRI improved the testicular microenvironment and alleviated age-related testosterone secretion insufficiency. These findings reveal the therapeutic potential of FOXO4-DRI for the treatment of male late-onset hypogonadism.
                ER  -

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DNAH10 mutation correlates with cisplatin sensitivity and tumor mutation burden in small-cell lung cancer

Man Li, Anqi Lin, Peng Luo, Weitao Shen, Dan Xiao, Lanying Gou, Jian Zhang, Linlang Guo,

https://doi.org/10.18632/aging.102683 pp 1285—1303

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Li M, Lin A, Luo P, Shen W, Xiao D, Gou L, Zhang J, Guo L, . DNAH10 mutation correlates with cisplatin sensitivity and tumor mutation burden in small-cell lung cancer. . 12:1285-1303. https://doi.org/10.18632/aging.102683

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Provider: 
 TY - JOUR
 AU - Li, Man 
 AU - Lin, Anqi 
 AU - Luo, Peng 
 AU - Shen, Weitao 
 AU - Xiao, Dan 
 AU - Gou, Lanying 
 AU - Zhang, Jian 
 AU - Guo, Linlang 
 TI - DNAH10 mutation correlates with cisplatin sensitivity and tumor mutation burden in small-cell lung cancer
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102683
 DO - 10.18632/aging.102683
 SP - 1285
 EP - 1303
 PY - 
 AB - Chemotherapies based on platinum have been the standard first-line treatment for patients with small-cell lung cancer(SCLC) in the past years. However, the progression of patients occurs mostly due to rapid development of resistance to chemotherapy. In addition, the mechanisms involved in development of cisplatin-resistance in SCLC remain undetermined. Here, we analyzed whole-exome sequencing(WES) datasets from Genomics of Drug Sensitivity in Cancer(GDSC, N=55) and WES data and overall survival(OS) from a published cohort(N=101) to search for cisplatin-resistant target genes and genes associated with poor prognosis. We use our cohort(NCT03162705) as the validation set. We applied single sample gene set enrichment analysis(ssGSEA) to explore the potential molecular mechanisms of cisplatin-resistance. DNAH10 mutations in SCLC was significantly associated with cisplatin-resistance(P=0.0350), poor OS(HR:3.445;P=0.00035) and worse progression-free survival (PFS)(P=0.0142). ssGSEA showed that the negative regulation of FGFR, the SPRY regulation of FGF, and the positive regulation of noncanonical WNT and PI3K/AKT/IKK signaling pathways are differentially up- or downregulated in DNAH10-mutated cell lines. A higher TMB was observed in DNAH10-mutated cell lines. Taken together, DNAH10 mutations may have a potential value in prediction of cisplatin resistance and poor survival in SCLC. Moreover, DNAH10 mutations may have a positive correlation with high TMB in SCLC.
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AURKB promotes gastric cancer progression via activation of CCND1 expression

Min Nie, Yadong Wang, Zenong Yu, Xinyu Li, Yexuan Deng, Ying Wang, Dongjun Yang, Qixiang Li, Xiangwei Zeng, Junyi Ju, Ming Liu, Quan Zhao,

https://doi.org/10.18632/aging.102684 pp 1304—1321

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Nie M, Wang Y, Yu Z, Li X, Deng Y, Wang Y, Yang D, Li Q, Zeng X, Ju J, Liu M, Zhao Q, . AURKB promotes gastric cancer progression via activation of CCND1 expression. . 12:1304-1321. https://doi.org/10.18632/aging.102684

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Provider: 
 TY - JOUR
 AU - Nie, Min 
 AU - Wang, Yadong 
 AU - Yu, Zenong 
 AU - Li, Xinyu 
 AU - Deng, Yexuan 
 AU - Wang, Ying 
 AU - Yang, Dongjun 
 AU - Li, Qixiang 
 AU - Zeng, Xiangwei 
 AU - Ju, Junyi 
 AU - Liu, Ming 
 AU - Zhao, Quan 
 TI - AURKB promotes gastric cancer progression via activation of CCND1 expression
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102684
 DO - 10.18632/aging.102684
 SP - 1304
 EP - 1321
 PY - 
 AB - Aurora kinase B (AURKB) triggers the phosphorylation of serine 10 on histone H3 (H3S10ph), which is important for chromosome condensation and cytokinesis during mitosis in mammals. However, how exactly AURKB controls cell cycle and contributes to tumorigenesis as an oncoprotein under pathological conditions remains largely unknown. Here, we report that AURKB promotes gastric cancer cell proliferation in vitro and in vivo. Silencing AURKB expression inhibits gastric cell proliferation and arrests the cell cycle in G2/M phase. We demonstrate that cyclin D1 (CCND1) is a direct downstream target of AURKB that plays a key role in gastric cancer cell proliferation. AURKB is able to activate the expression of CCND1 through mediating H3S10ph in the promoter of the CCND1 gene. Furthermore, we show that AZD1152, a specific inhibitor of AURKB, can suppress the expression of CCND1 in the gastric cancer cells and inhibit cell proliferation in vitro and in vivo. Importantly, we found that high AURKB and CCND1 expression levels are correlated with shorter overall survival of gastric cancer patients. This study demonstrates that AURKB promotes gastric tumorigenesis potentially through epigenetically activating CCND1 expression, suggesting AURKB as a promising therapeutic target in gastric cancer.
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Association of antinuclear antibodies with the risk of intracranial arterial stenosis

Yong-An Sun, Qiu Han, Xiao-He Hou, Xian-Zhen Peng, Lin Tong, Xu Zheng, Jin-Tai Yu, Lan Tan,

https://doi.org/10.18632/aging.102685 pp 1322—1331

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Sun Y, Han Q, Hou X, Peng X, Tong L, Zheng X, Yu J, Tan L, . Association of antinuclear antibodies with the risk of intracranial arterial stenosis. . 12:1322-1331. https://doi.org/10.18632/aging.102685

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                TY  - JOUR
                AU  - Sun, Yong-An 
                AU  - Han, Qiu 
                AU  - Hou, Xiao-He 
                AU  - Peng, Xian-Zhen 
                AU  - Tong, Lin 
                AU  - Zheng, Xu 
                AU  - Yu, Jin-Tai 
                AU  - Tan, Lan 
                TI  - Association of antinuclear antibodies with the risk of intracranial arterial stenosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102685
                DO  - 10.18632/aging.102685
                SP  - 1322
                EP  - 1331
                PY  - 
                AB  - The prevalence of intracranial arterial stenosis (IAS) as well as antinuclear antibody (ANA) positivity was found to be higher in Asians than that in the Western population. To investigate the relation of ANAs with IAS in patients with acute ischemic cerebrovascular disease, we enrolled 2492 patients with acute ischemic stroke or transient ischemic attack into the study. All the patients were categorized into 3 groups according to the IAS burden. Multinomial logistic regression analyses were used in statistical analysis. The positive rate of ANAs in the IAS &#x2265; 2 group was higher than that in the single IAS group and the no IAS group (p&lt;0.001). The adjusted odds ratio (OR) for IAS &#x2265; 2 in ANAs-positive patients was 3.737 (95%CI=2.676-5.220, p&lt;0.001) compared with the ANAs-negative patients. ANAs were associated with multiple IAS rather than single IAS in both male and female subgroups. Besides, ANAs were significantly associated with single and multiple IAS in individuals &#x2264; 60 years. However, ANAs were only associated with two or more IAS in two age groups (between 61 to 75 years and &gt;75 years old). In summary, ANAs are associated with IAS in patients with acute ischemic cerebrovascular disease.
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Identification of key genes by integrating DNA methylation and next-generation transcriptome sequencing for esophageal squamous cell carcinoma

Yang Chen, Lian-Di Liao, Zhi-Yong Wu, Qian Yang, Jin-Cheng Guo, Jian-Zhong He, Shao-Hong Wang, Xiu-E Xu, Jian-Yi Wu, Feng Pan, De-Chen Lin, Li-Yan Xu, En-Min Li,

https://doi.org/10.18632/aging.102686 pp 1332—1365

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Chen Y, Liao L, Wu Z, Yang Q, Guo J, He J, Wang S, Xu X, Wu J, Pan F, Lin D, Xu L, Li E, . Identification of key genes by integrating DNA methylation and next-generation transcriptome sequencing for esophageal squamous cell carcinoma. . 12:1332-1365. https://doi.org/10.18632/aging.102686

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                TY  - JOUR
                AU  - Chen, Yang 
                AU  - Liao, Lian-Di 
                AU  - Wu, Zhi-Yong 
                AU  - Yang, Qian 
                AU  - Guo, Jin-Cheng 
                AU  - He, Jian-Zhong 
                AU  - Wang, Shao-Hong 
                AU  - Xu, Xiu-E 
                AU  - Wu, Jian-Yi 
                AU  - Pan, Feng 
                AU  - Lin, De-Chen 
                AU  - Xu, Li-Yan 
                AU  - Li, En-Min 
                TI  - Identification of key genes by integrating DNA methylation and next-generation transcriptome sequencing for esophageal squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102686
                DO  - 10.18632/aging.102686
                SP  - 1332
                EP  - 1365
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Chen, Yang 
                AU  - Liao, Lian-Di 
                AU  - Wu, Zhi-Yong 
                AU  - Yang, Qian 
                AU  - Guo, Jin-Cheng 
                AU  - He, Jian-Zhong 
                AU  - Wang, Shao-Hong 
                AU  - Xu, Xiu-E 
                AU  - Wu, Jian-Yi 
                AU  - Pan, Feng 
                AU  - Lin, De-Chen 
                AU  - Xu, Li-Yan 
                AU  - Li, En-Min 
                TI  - Identification of key genes by integrating DNA methylation and next-generation transcriptome sequencing for esophageal squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102686
                DO  - 10.18632/aging.102686
                SP  - 1332
                EP  - 1365
                PY  - 
                AB  - Aberrant DNA methylation leads to abnormal gene expression, making it a significant regulator in the progression of cancer and leading to the requirement for integration of gene expression with DNA methylation. Here, we identified 120 genes demonstrating an inverse correlation between DNA methylation and mRNA expression in esophageal squamous cell carcinoma (ESCC). Sixteen key genes, such as SIX4, CRABP2, and EHD3, were obtained by filtering 10 datasets and verified in paired ESCC samples by qRT-PCR. 5-Aza-dC as a DNA methyltransferase (DNMT) inhibitor could recover their expression and inhibit clonal growth of cancer cells in seven ESCC cell lines. Furthermore, 11 of the 16 genes were correlated with OS (overall survival) and DFS (disease-free survival) in 125 ESCC patients. ChIP-Seq data and WGBS data showed that DNA methylation and H3K27ac histone modification of these key genes displayed inverse trends, suggesting that there was collaboration between DNA methylation and histone modification in ESCC. Our findings illustrate that the integrated multi-omics data (transcriptome and epigenomics) can accurately obtain potential prognostic biomarkers, which may provide important insight for the effective treatment of cancers.
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Development of prognostic index based on autophagy-related genes analysis in breast cancer

Qing-Guang Lin, Wei Liu, Yu-zhen Mo, Jing Han, Zhi-Xing Guo, Wei Zheng, Jian-wei Wang, Xue-Bin Zou, An-Hua Li, Feng Han,

https://doi.org/10.18632/aging.102687 pp 1366—1376

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Lin Q, Liu W, Mo Y, Han J, Guo Z, Zheng W, Wang J, Zou X, Li A, Han F, . Development of prognostic index based on autophagy-related genes analysis in breast cancer. . 12:1366-1376. https://doi.org/10.18632/aging.102687

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                TY  - JOUR
                AU  - Lin, Qing-Guang 
                AU  - Liu, Wei 
                AU  - Mo, Yu-zhen 
                AU  - Han, Jing 
                AU  - Guo, Zhi-Xing 
                AU  - Zheng, Wei 
                AU  - Wang, Jian-wei 
                AU  - Zou, Xue-Bin 
                AU  - Li, An-Hua 
                AU  - Han, Feng 
                TI  - Development of prognostic index based on autophagy-related genes analysis in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102687
                DO  - 10.18632/aging.102687
                SP  - 1366
                EP  - 1376
                PY  - 
                AB  - Background: Autophagy is a self-digesting process that can satisfy the metabolic needs of cells, and is closely related to development of cancer. However, the effect of autophagy-related genes (ARGs) on the prognosis of breast cancer remains unclear.Results: We first found that 27 ARGs were significantly associated with overall survival in breast cancer. The prognosis-related ARGs signature established using the Cox regression model consists of 12 ARGs that can be divided patients into high-risk and low-risk groups. The overall survival of patients with high-risk scores (HR 3.652, 2.410-5.533; P &lt; 0.001) was shorter than patients with low-risk scores. The area under the receiver operating characteristic (ROC) curve for 1-year, 3-year, and 5-year survival rates were 0.739, 0.727, and 0.742, respectively.Conclusion: The12-ARGs marker can predict the prognosis of breast cancer and thus help individualized treatment of patients at different risks.Methods: Based on the TCGA dataset, we integrated the expression profiles of ARGs in 1,039 breast cancer patients. Differentially expressed ARGs and survival-related ARGs were evaluated by computational difference algorithm and COX regression analysis. In addition, we also explored the mutations in these ARGs. A new prognostic indicator based on ARGs was developed using multivariate COX analysis.
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The role of serum growth hormone and insulin-like growth factor-1 in adult humans brain morphology

Taoyang Yuan, Jianyou Ying, Lu Jin, Chuzhong Li, Songbai Gui, Zhenye Li, Rui Wang, Zhentao Zuo, Yazhuo Zhang,

https://doi.org/10.18632/aging.102688 pp 1377—1396

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Yuan T, Ying J, Jin L, Li C, Gui S, Li Z, Wang R, Zuo Z, Zhang Y, . The role of serum growth hormone and insulin-like growth factor-1 in adult humans brain morphology. . 12:1377-1396. https://doi.org/10.18632/aging.102688

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                TY  - JOUR
                AU  - Yuan, Taoyang 
                AU  - Ying, Jianyou 
                AU  - Jin, Lu 
                AU  - Li, Chuzhong 
                AU  - Gui, Songbai 
                AU  - Li, Zhenye 
                AU  - Wang, Rui 
                AU  - Zuo, Zhentao 
                AU  - Zhang, Yazhuo 
                TI  - The role of serum growth hormone and insulin-like growth factor-1 in adult humans brain morphology
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102688
                DO  - 10.18632/aging.102688
                SP  - 1377
                EP  - 1396
                PY  - 
                AB  - Growth hormone (GH) and its anabolic mediator, insulin-like growth factor-1 (IGF-1), have a critical role in the central nervous system. However, their detailed roles in the adult human brain are not clear. In this study, structural MRIs of 48 patients with GH-secreting pituitary adenoma (GH-PA), 48 sex- and age-matched clinical Non-Functional pituitary adenoma patients (NonFun-PA) and healthy controls (HCs) were assessed using voxel-based morphometry (VBM) and region-based morphometry (RBM). Correlation analyses helped determine the relationships between serum hormone levels and brain structure. The whole-brain gray matter volume (GMV) and white matter volume (WMV) significantly increased at the expense of cerebrospinal fluid volume (CSFV) in GH-PA (Bonferroni corrected, p&lt;0.01). The increase in GMV and reduction in CSFV were significantly correlated with serum GH/IGF-1 levels (p&lt;0.05). VBM showed significant correlations of the GMV/WMV alteration pattern between GH-PA vs HCs and GH-PA vs NonFun-PA and widespread bilateral clusters of significantly increased GMV and WMV in GH-PA (pFDR&lt;0.05). RBM showed obviously increased GMV/WMV in 54 of 68 brain regions (p&lt;0.05) in GH-PA compared to HCs. Our results provide imaging evidence that serum GH/IGF-1 contributes to brain growth, which may be a potential treatment option for neurodegenerative disorders and brain injury in humans.
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Activated Drp1-mediated mitochondrial ROS influence the gut microbiome and intestinal barrier after hemorrhagic shock

Chenyang Duan, Lei Kuang, Xinming Xiang, Jie Zhang, Yu Zhu, Yue Wu, Qingguang Yan, Liangming Liu, Tao Li,

https://doi.org/10.18632/aging.102690 pp 1397—1416

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Duan C, Kuang L, Xiang X, Zhang J, Zhu Y, Wu Y, Yan Q, Liu L, Li T, . Activated Drp1-mediated mitochondrial ROS influence the gut microbiome and intestinal barrier after hemorrhagic shock. . 12:1397-1416. https://doi.org/10.18632/aging.102690

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                TY  - JOUR
                AU  - Duan, Chenyang 
                AU  - Kuang, Lei 
                AU  - Xiang, Xinming 
                AU  - Zhang, Jie 
                AU  - Zhu, Yu 
                AU  - Wu, Yue 
                AU  - Yan, Qingguang 
                AU  - Liu, Liangming 
                AU  - Li, Tao 
                TI  - Activated Drp1-mediated mitochondrial ROS influence the gut microbiome and intestinal barrier after hemorrhagic shock
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102690
                DO  - 10.18632/aging.102690
                SP  - 1397
                EP  - 1416
                PY  - 
                AB  - A role of the mitochondrial dynamin-related protein (Drp1) on gut microbiome composition and intestinal barrier function after hemorrhagic shock has not been identified previously and thus addressed in this study. Here, we used a combination of 16S rRNA gene sequencing and mass spectrometry-based metabolomics profiling in WT and Drp1 KO mouse models to examine the functional impact of activated Drp1 on the gut microbiome as well as mitochondrial metabolic regulation after hemorrhagic shock. Our data showed that changes in mitochondrial Drp1 activity participated in the regulation of intestinal barrier function after hemorrhagic shock. Activated Drp1 significantly perturbed gut microbiome composition in the Bacteroidetes phylum. The abundance of short-chain fatty acid (SCFA) producing microbes, such as Bacteroides, Butyricimonas and Odoribacter, was markedly decreased in mice after shock, and was inversely correlated with both the distribution of the tight junction protein ZO1 and intestinal permeability. Together, these data suggest that Drp1 activation perturbs the gut microbiome community and SCFA production in a ROS-specific manner and thereby substantially disturbs tight junctions and intestinal barrier function after hemorrhagic shock. Our findings provide novel insights for targeting Drp1-mediated mitochondrial function as well as the microbiome in the treatment of intestinal barrier dysfunction after shock.
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SRV2 promotes mitochondrial fission and Mst1-Drp1 signaling in LPS-induced septic cardiomyopathy

Xiuling Shang, Yingrui Zhang, Jingqing Xu, Min Li, Xiaoting Wang, Rongguo Yu,

https://doi.org/10.18632/aging.102691 pp 1417—1432

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Shang X, Zhang Y, Xu J, Li M, Wang X, Yu R, . SRV2 promotes mitochondrial fission and Mst1-Drp1 signaling in LPS-induced septic cardiomyopathy. . 12:1417-1432. https://doi.org/10.18632/aging.102691

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                TY  - JOUR
                AU  - Shang, Xiuling 
                AU  - Zhang, Yingrui 
                AU  - Xu, Jingqing 
                AU  - Li, Min 
                AU  - Wang, Xiaoting 
                AU  - Yu, Rongguo 
                TI  - SRV2 promotes mitochondrial fission and Mst1-Drp1 signaling in LPS-induced septic cardiomyopathy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102691
                DO  - 10.18632/aging.102691
                SP  - 1417
                EP  - 1432
                PY  - 
                AB  - Mitochondrial fission is associated with cardiomyocyte death and myocardial depression, and suppressor of ras val-2 (SRV2) is a newly discovered pro-fission protein. In this study, we examined the mechanisms of SRV2-mediated mitochondrial fission in septic cardiomyopathy. Western blotting, ELISA, and immunofluorescence were used to evaluate mitochondrial function, oxidative balance, energy metabolism and caspase-related death, and siRNA and adenoviruses were used to perform loss- and gain-of-function assays. Our results demonstrated that increased SRV2 expression promotes, while SRV2 knockdown attenuates, cardiomyocyte death in LPS-induced septic cardiomyopathy. Mechanistically, SRV2 activation promoted mitochondrial fission and physiological abnormalities by upregulating oxidative injury, ATP depletion, and caspase-9-related apoptosis. Our results also demonstrated that SRV2 promotes mitochondrial fission via a Mst1-Drp1 axis. SRV2 knockdown decreased Mst1 and Drp1 levels, while Mst1 overexpression abolished the mitochondrial protection and cardiomyocyte survival-promoting effects of SRV2 knockdown. SRV2 is thus a key novel promotor of mitochondrial fission and Mst1-Drp1 axis activity in septic cardiomyopathy.
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Association between TNF-alpha polymorphism and the age of first suicide attempt in chronic patients with schizophrenia

Xiaoe Lang, Tammy H. Trihn, Hanjing Emily Wu, Yongsheng Tong, Meihong Xiu, Xiang Yang Zhang,

https://doi.org/10.18632/aging.102692 pp 1433—1445

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Lang X, Trihn TH, Wu HE, Tong Y, Xiu M, Zhang XY, . Association between TNF-alpha polymorphism and the age of first suicide attempt in chronic patients with schizophrenia. . 12:1433-1445. https://doi.org/10.18632/aging.102692

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Provider: 
 TY - JOUR
 AU - Lang, Xiaoe 
 AU - Trihn, Tammy H. 
 AU - Wu, Hanjing Emily 
 AU - Tong, Yongsheng 
 AU - Xiu, Meihong 
 AU - Zhang, Xiang Yang 
 TI - Association between TNF-alpha polymorphism and the age of first suicide attempt in chronic patients with schizophrenia
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102692
 DO - 10.18632/aging.102692
 SP - 1433
 EP - 1445
 PY - 
 AB - Patients with schizophrenia (SCZ) exhibit higher suicide rates than the general population. However, the molecular mechanism remains poorly understood. Tumor necrosis factor (TNF)-alpha polymorphisms have been repeatedly indicated to play a pathogenetic role in various mental disorders, but none of these studies focused on the susceptibility to suicidal behavior in SCZ. We recruited 1087 chronic inpatients with SCZ and 576 controls to assess the psychopathological symptoms of SCZ using the Positive and Negative Syndrome Scale scales. We selected 2 polymorphisms (-308G&gt;A and -1031C&gt;T) in the TNF-alpha gene and analyzed their associations with SCZ and suicide. Our results showed that TNF-alpha -308G&gt;A and -1031C&gt;T were not related to SCZ and suicide. However, we found that suicide attempters with the C allele carriers exhibited suicidal behaviors significantly later than those with TT genotype in the SCZ patients. The haplotype containing the T allele of the -1031 was significantly associated with the age of suicide initiation. Further logistic regression analysis showed that -1031C&gt;T interacted with psychopathological symptoms and drinking, age of smoking, and related to the initiation age of suicide attempts. Our study demonstrated that the TNF-alpha variants may affect the age at which suicide attempts started among SCZ suicide attempters.
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Immunological analyses reveal an immune subtype of uveal melanoma with a poor prognosis

Hui Pan, Linna Lu, Junqi Cui, Yuan Yang, Zhaoyang Wang, Xianqun Fan,

https://doi.org/10.18632/aging.102693 pp 1446—1464

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Pan H, Lu L, Cui J, Yang Y, Wang Z, Fan X, . Immunological analyses reveal an immune subtype of uveal melanoma with a poor prognosis. . 12:1446-1464. https://doi.org/10.18632/aging.102693

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                TY  - JOUR
                AU  - Pan, Hui 
                AU  - Lu, Linna 
                AU  - Cui, Junqi 
                AU  - Yang, Yuan 
                AU  - Wang, Zhaoyang 
                AU  - Fan, Xianqun 
                TI  - Immunological analyses reveal an immune subtype of uveal melanoma with a poor prognosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102693
                DO  - 10.18632/aging.102693
                SP  - 1446
                EP  - 1464
                PY  - 
                AB  - Uveal melanoma is an aggressive intraocular malignancy that often exhibits low immunogenicity. Metastatic uveal melanoma samples frequently exhibit monosomy 3 or BAP1 deficiency. In this study, we used bioinformatic methods to investigate the immune infiltration of uveal melanoma samples in public datasets. We first performed Gene Set Enrichment/Variation Analyses to detect immunological pathways that are altered in tumors with monosomy 3 or BAP1 deficiency. We then conducted an unsupervised clustering analysis to identify distinct immunologic molecular subtypes of uveal melanoma. We used CIBERSORT and ESTIMATE with RNA-seq data from The Cancer Genome Atlas and the GSE22138 microarray dataset to determine the sample-level immune subpopulations and immune scores of uveal melanoma samples. The Kaplan-Meier method and log-rank test were used to assess the prognostic value of particular immune cells and genes in uveal melanoma samples. Through these approaches, we discovered uveal melanoma-specific immunologic features, which may provide new insights into the tumor microenvironment and enhance the development of immunotherapies in the future.
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MTDH promotes metastasis of clear cell renal cell carcinoma by activating SND1-mediated ERK signaling and epithelial-mesenchymal transition

Anbang He, Shiming He, Cong Huang, Zhicong Chen, Yucai Wu, Yanqing Gong, Xuesong Li, Liqun Zhou,

https://doi.org/10.18632/aging.102694 pp 1465—1487

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He A, He S, Huang C, Chen Z, Wu Y, Gong Y, Li X, Zhou L, . MTDH promotes metastasis of clear cell renal cell carcinoma by activating SND1-mediated ERK signaling and epithelial-mesenchymal transition. . 12:1465-1487. https://doi.org/10.18632/aging.102694

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                TY  - JOUR
                AU  - He, Anbang 
                AU  - He, Shiming 
                AU  - Huang, Cong 
                AU  - Chen, Zhicong 
                AU  - Wu, Yucai 
                AU  - Gong, Yanqing 
                AU  - Li, Xuesong 
                AU  - Zhou, Liqun 
                TI  - MTDH promotes metastasis of clear cell renal cell carcinoma by activating SND1-mediated ERK signaling and epithelial-mesenchymal transition
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102694
                DO  - 10.18632/aging.102694
                SP  - 1465
                EP  - 1487
                PY  - 
                AB  - Background: Metastasis is the principal cause of renal cell carcinoma-associated mortality. Metadherin (MTDH) was identified as a vital metastasis driver involved in the metastatic progression of various types of tumors, suggesting that MTDH is a prognostic metastatic biomarker and potential therapeutic target. The role and mechanism of MTDH in the metastatic progression of ccRCC have not yet been adequately explored.Results: MTDH was remarkably elevated in ccRCC tissues, especially in metastatic ccRCC tissues, compared with normal kidney tissues and correlated with advanced clinicopathological features and poor prognosis. MTDH activated ERK signaling and EMT, thus promoting the migration and invasion of ccRCC cells. The interaction between MTDH and SND1 at the protein level was confirmed using immunoprecipitation and immunofluorescence. Based on the analysis of datasets from GEO and TCGA, SND1 was remarkably increased in ccRCC, especially in metastatic ccRCC, and associated with advanced clinicopathological features and poor prognosis. Knockdown of SND1 mainly abolished the migration and invasion of ccRCC cells by blocking MTDH-mediated ERK and EMT signaling activation.Conclusion: These results revealed that MTDH may be a prognostic metastatic biomarker of ccRCC that promotes ccRCC metastasis by activating SND1-mediated the ERK and EMT signaling pathways. MTDH may serve as an anti-tumor therapeutic target that can be applied for the clinical treatment of metastatic ccRCC.Methods: MTDH/SND1 mRNA expression in clear cell renal cell carcinoma (ccRCC) was comprehensively estimated by analysis of GEO-ccRCC and TCGA-KIRC datasets with R software and packages. MTDH protein expression was assessed in a total of 111 ccRCC patients from Peking University First Hospital by immunohistochemistry (IHC). In vitro migration and invasion assays were carried out, and an in vivo metastatic mouse model was developed to investigate the biological functions of MTDH in ccRCC cells. Correlation analysis, immunoprecipitation, western blotting and immunofluorescence were applied to explore the molecular mechanisms of MTDH in ccRCC.
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Plasma ubiquitin C-terminal hydrolase L1 levels reflect disease stage and motor severity in Parkinson’s disease

Adeline Su Lyn Ng, Yi Jayne Tan, Zhonghao Lu, Ebonne Yulin Ng, Samuel Yong Ern Ng, Nicole Shuang Yu Chia, Fiona Setiawan, Zheyu Xu, Nicole Chwee Har Keong, Kay Yaw Tay, Wing Lok Au, Louis Chew Seng Tan, Eng-King Tan,

https://doi.org/10.18632/aging.102695 pp 1488—1495

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Ng ASL, Tan YJ, Lu Z, Ng EY, Ng SYE, Chia NSY, Setiawan F, Xu Z, Keong NCH, Tay KY, Au WL, Tan LCS, Tan E, . Plasma ubiquitin C-terminal hydrolase L1 levels reflect disease stage and motor severity in Parkinson’s disease. . 12:1488-1495. https://doi.org/10.18632/aging.102695

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                TY  - JOUR
                AU  - Ng, Adeline Su Lyn 
                AU  - Tan, Yi Jayne 
                AU  - Lu, Zhonghao 
                AU  - Ng, Ebonne Yulin 
                AU  - Ng, Samuel Yong Ern 
                AU  - Chia, Nicole Shuang Yu 
                AU  - Setiawan, Fiona 
                AU  - Xu, Zheyu 
                AU  - Keong, Nicole Chwee Har 
                AU  - Tay, Kay Yaw 
                AU  - Au, Wing Lok 
                AU  - Tan, Louis Chew Seng 
                AU  - Tan, Eng-King 
                TI  - Plasma ubiquitin C-terminal hydrolase L1 levels reflect disease stage and motor severity in Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102695
                DO  - 10.18632/aging.102695
                SP  - 1488
                EP  - 1495
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ng, Adeline Su Lyn 
                AU  - Tan, Yi Jayne 
                AU  - Lu, Zhonghao 
                AU  - Ng, Ebonne Yulin 
                AU  - Ng, Samuel Yong Ern 
                AU  - Chia, Nicole Shuang Yu 
                AU  - Setiawan, Fiona 
                AU  - Xu, Zheyu 
                AU  - Keong, Nicole Chwee Har 
                AU  - Tay, Kay Yaw 
                AU  - Au, Wing Lok 
                AU  - Tan, Louis Chew Seng 
                AU  - Tan, Eng-King 
                TI  - Plasma ubiquitin C-terminal hydrolase L1 levels reflect disease stage and motor severity in Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102695
                DO  - 10.18632/aging.102695
                SP  - 1488
                EP  - 1495
                PY  - 
                AB  - Parkinson&#x2019;s disease (PD) is characterized by Lewy bodies containing &#x3B1;-synuclein and ubiquitin aggregates, their co-occurrence possibly linked to a failure of the ubiquitin proteasome system. Ubiquitin C-terminal hydrolase L1 (UCHL1) plays an important role in maintenance of nervous system integrity, and overexpression of UCHL1 has been shown to increase ubiquitin levels within neurons. While cerebrospinal fluid ubiquitin levels were reported to be lower in PD vs controls, plasma UCHL1 levels and their relationship with clinical measures in PD has not been reported. We measured plasma UCHL1 levels using single molecule array (Simoa) in 291 subjects (242 PD and 49 healthy controls, HC). We found that UCHL1 levels were significantly higher in PD patients at moderate stages (Hoehn and Yahr, H&amp;Y stage &gt;2) vs milder PD (H&amp;Y &#x2264;2, p&lt;0.001) and HC (p=0.001). There was no significant difference in UCHL1 levels between PD patients at H&amp;Y stages &#x2264;2 vs HC. Across all PD patients, UCHL1 correlated significantly with UPDRS Part III motor scores (&#x3B2;=3.87, 95% CI=0.43-7.31, p=0.028), but not with global cognition. Overall, we found that UCHL1 correlates with motor function in PD, with higher levels seen in later disease stages. These findings will be validated in longitudinal studies.
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Association of cardiovascular structure and function with cerebrovascular changes and cognitive function in older patients with end-stage renal disease

Laurien E. Zijlstra, Stella Trompet, J. Wouter Jukema, Lucia J. M. Kroft, Jeroen de Bresser, Matthias J. P. van Osch, Sebastiaan Hammer, Marie-Noëlle Witjes, Marjolijn van Buren, Simon P. Mooijaart,

https://doi.org/10.18632/aging.102696 pp 1496—1511

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Zijlstra LE, Trompet S, Jukema JW, Kroft LJM, de Bresser J, van Osch MJP, Hammer S, Witjes M, van Buren M, Mooijaart SP, . Association of cardiovascular structure and function with cerebrovascular changes and cognitive function in older patients with end-stage renal disease. . 12:1496-1511. https://doi.org/10.18632/aging.102696

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                TY  - JOUR
                AU  - Zijlstra, Laurien E. 
                AU  - Trompet, Stella 
                AU  - Jukema, J. Wouter 
                AU  - Kroft, Lucia J. M. 
                AU  - de Bresser, Jeroen 
                AU  - van Osch, Matthias J. P. 
                AU  - Hammer, Sebastiaan 
                AU  - Witjes, Marie-Noëlle 
                AU  - van Buren, Marjolijn 
                AU  - Mooijaart, Simon P. 
                TI  - Association of cardiovascular structure and function with cerebrovascular changes and cognitive function in older patients with end-stage renal disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102696
                DO  - 10.18632/aging.102696
                SP  - 1496
                EP  - 1511
                PY  - 
                AB  - The Dutch prospective multicenter cohort study COPE (Cognitive decline in Older Patients with End stage renal disease) aimed to investigate the association of cardiovascular structure and function with cerebrovascular changes and cognitive function in 85 older patients with chronic kidney disease stage 4 and 5, awaiting either dialysis or conservative care. MRI was performed measuring aortic stiffness (pulse wave velocity [PWV]) and cardiac systolic function (ejection fraction and cardiac index). Outcomes were MRI-derived cerebrovascular changes (microbleeds, lacunes and white matter hyperintensities) and cognitive function (memory, executive function and psychomotor speed). Mean age was 76 years and 66% were male. No statistically significant associations were observed between cardiovascular parameters and cerebrovascular changes. Cognitive function was worse in patients with high compared to low PWV in all three cognitive domains. Although there were clinically relevant associations of high PWV with poor cognition in all domains, after adjustment for age, sex and education only the Trail Making Test A remained statistically significant (p=0.030). In conclusion, this study suggests that a higher PWV might be associated with lower cognitive function, suggesting that arterial stiffness may be an underlying mechanism of development of cognitive impairment in older patients with ESRD. Larger studies should replicate and extend these findings.
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Identification of a nomogram based on long non-coding RNA to improve prognosis prediction of esophageal squamous cell carcinoma

Wenli Li, Jun Liu, Hetong Zhao,

https://doi.org/10.18632/aging.102697 pp 1512—1526

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Li W, Liu J, Zhao H, . Identification of a nomogram based on long non-coding RNA to improve prognosis prediction of esophageal squamous cell carcinoma. . 12:1512-1526. https://doi.org/10.18632/aging.102697

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                TY  - JOUR
                AU  - Li, Wenli 
                AU  - Liu, Jun 
                AU  - Zhao, Hetong 
                TI  - Identification of a nomogram based on long non-coding RNA to improve prognosis prediction of esophageal squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102697
                DO  - 10.18632/aging.102697
                SP  - 1512
                EP  - 1526
                PY  - 
                AB  - Purpose: Esophageal squamous cell carcinoma (ESCC) remains a common aggressive malignancy in the world. Several long non-coding RNAs (lncRNAs) are reported to predict the prognosis of ESCC. Therefore, an in-depth research is urgently needed to further investigate the prognostic value of lncRNAs in ESCC.Results: From the training set, we identified a eight-lncRNA signature (including AP000487, AC011997, LINC01592, LINC01497, LINC01711, FENDRR, AC087045, AC137770) which separated the patients into two groups with significantly different overall survival (hazard ratio, HR = 3.79, 95% confidence interval, 95% CI [2.56-5.62]; P &lt; 0.001). The signature was applied to the validation set (HR = 2.73, 95%CI [1.65-4.53]; P &lt; 0.001) and showed similar prognostic values. Stratified, univariate and multivariate Cox regression analysis indicated that the signature was an independent prognostic factor for patients with ESCC. A nomogram based on the lncRNAs signature, age, grade and stage was developed and showed good accuracy for predicting 1-, 3- and 5-year survival probability of ESCC patients. We found a strong correlation between the gene significance for the survival time and T stage. Eight modules were constructed, among which the key module most closely associated with clinical information was identified.Conclusions: Our eight-lincRNA signature and nomogram could be practical and reliable prognostic tools for esophageal squamous cell carcinoma.Methods: We downloaded the lncRNA expression profiles of ESCC patients from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets and separated to training and validation cohort. The univariate, least absolute shrinkage and selection operator (LASSO) and multivariate Cox regression analysis were used to identify a lncRNA-based signature. The predictive value of the signature was assessed using the Kaplan-Meier method, receiver operating characteristic (ROC) curves and area under curve (AUC). Weighted gene co-expression network analysis (WGCNA) was applied to predict the intrinsic relationship between gene expressions. In addition, we further explored the combination of clinical information and module construction.
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Aquaporin 9 inhibits growth and metastasis of hepatocellular carcinoma cells via Wnt/β-catenin pathway

Shengtao Liao, Hongyu Chen, Min Liu, Li Gan, Chuanfei Li, Wenguang Zhang, Lin Lv, Zhechuan Mei,

https://doi.org/10.18632/aging.102698 pp 1527—1544

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Liao S, Chen H, Liu M, Gan L, Li C, Zhang W, Lv L, Mei Z, . Aquaporin 9 inhibits growth and metastasis of hepatocellular carcinoma cells via Wnt/β-catenin pathway. . 12:1527-1544. https://doi.org/10.18632/aging.102698

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                TY  - JOUR
                AU  - Liao, Shengtao 
                AU  - Chen, Hongyu 
                AU  - Liu, Min 
                AU  - Gan, Li 
                AU  - Li, Chuanfei 
                AU  - Zhang, Wenguang 
                AU  - Lv, Lin 
                AU  - Mei, Zhechuan 
                TI  - Aquaporin 9 inhibits growth and metastasis of hepatocellular carcinoma cells via Wnt/β-catenin pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102698
                DO  - 10.18632/aging.102698
                SP  - 1527
                EP  - 1544
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is the most common type of liver cancer worldwide, and it is the second leading cause of cancer-related mortality. Aquaporin 9 (AQP9) is an essential aquaporin in the liver and located in the basolateral membrane of hepatocytes, but its roles on HCC has not been completely elucidated. This study investigated the regulatory functions of AQP9 in the pathogenesis of HCC. The expression levels of AQP9 were significantly down-regulated in HCC tissues and cells, which was also correlated with tumor size and number, TNM stage, five-year survival rate, lymphatic and distal metastasis within the patients. Furthermore, overexpressed AQP9 suppressed the proliferation, migration and invasion of HCC cells. The levels of PCNA, E-cad, N-cad, &#x3B1;-SMA, DVL2, GSK-3&#x3B2;, cyclinD1 and &#x3B2;-catenin in HCC cells were reduced by overexpressed AQP9, while cell apoptosis was remarkably enhanced. Additionally, following the treatment with Wnt/&#x3B2;-catenin signaling inhibitor (XAV939), the proliferative activity of HCC cells was significantly inhibited; PCNA and EMT-related markers were down-regulated; migration and invasion of cells were notably suppressed; cell apoptotic rate was decreased. Vice versa, after the cells were treated with Wnt/&#x3B2;-catenin inducer (SKL2001), the effects caused by overexpressed AQP9 were abrogated. In vivo studies indicated that tumor volume and weight were remarkably decreased in AQP9 overexpression group, where the levels of Wnt/&#x3B2;-catenin signaling- and EMT-associated molecules were also reduced. Taken together, our results suggested that overexpressed AQP9 could inhibit growth and metastasis of HCC cells via Wnt/&#x3B2;-catenin pathway. AQP9 may be a promising therapeutic target for the treatment of patients with HCC.
                ER  -

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Antihypertensive medications are associated with the risk of kidney and bladder cancer: a systematic review and meta-analysis

Yuxiu Xie, Peng Xu, Meng Wang, Yi Zheng, Tian Tian, Si Yang, Yujiao Deng, Ying Wu, Zhen Zhai, Qian Hao, Dingli Song, Dai Zhang, Zhijun Dai,

https://doi.org/10.18632/aging.102699 pp 1545—1562

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Xie Y, Xu P, Wang M, Zheng Y, Tian T, Yang S, Deng Y, Wu Y, Zhai Z, Hao Q, Song D, Zhang D, Dai Z, . Antihypertensive medications are associated with the risk of kidney and bladder cancer: a systematic review and meta-analysis. . 12:1545-1562. https://doi.org/10.18632/aging.102699

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                TY  - JOUR
                AU  - Xie, Yuxiu 
                AU  - Xu, Peng 
                AU  - Wang, Meng 
                AU  - Zheng, Yi 
                AU  - Tian, Tian 
                AU  - Yang, Si 
                AU  - Deng, Yujiao 
                AU  - Wu, Ying 
                AU  - Zhai, Zhen 
                AU  - Hao, Qian 
                AU  - Song, Dingli 
                AU  - Zhang, Dai 
                AU  - Dai, Zhijun 
                TI  - Antihypertensive medications are associated with the risk of kidney and bladder cancer: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102699
                DO  - 10.18632/aging.102699
                SP  - 1545
                EP  - 1562
                PY  - 
                AB  - Several studies have indicated that the use of antihypertensive medications may influence the incidence of bladder/kidney cancer, with some scholars refuting any such association. Hence, a systematic review is needed to verify this linkage. we comprehensively searched PubMed, Embase, Web of Science, and the Cochrane Library for original studies reporting a relationship between antihypertensive medications and risk of bladder/kidney cancer. We included 31 articles comprising 3,352,264 participants. We found a significant association between the risk of kidney cancer and any antihypertensive medications use (relative risk (RR) = 1.45, 95% CI 1.20-1.75), as well as angiotensin-converting enzyme inhibitors (RR = 1.24, 95% CI 1.04-1.48), angiotensin II receptor blockers (ARB) (RR = 1.29, 95% CI:1.22-1.37), beta-blockers (RR = 1.36, 95% CI 1.11-1.66), calcium-channel blockers (RR = 1.65, 95% CI 1.54-1.78) and diuretics (RR = 1.34, 95% CI 1.19-1.51). In case of bladder cancer, a statistical significance was observed with the use of ARB (RR = 1.07, 95% CI 1.03-1.11) but not with the other antihypertensive medications. There was a linear association between the duration of antihypertensive medications and the risk of kidney cancer (P = 0.061 for a non-linear trend) and the pooled RR for the per year increase in antihypertensive medications duration of use was 1.02 (95% CI: 1.01-1.02). Our results indicate that there is a significant association between each class of antihypertensive medications and the risk of kidney cancer, and this trend presented as a positive linear association. Furthermore, the use of ARB has been linked to the risk of bladder cancer.
                ER  -

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SENP1 is a crucial promotor for hepatocellular carcinoma through deSUMOylation of UBE2T

Yifeng Tao, Ruidong Li, Conghuan Shen, Jianhua Li, Quanbao Zhang, Zhenyu Ma, Feifei Wang, Zhengxin Wang,

https://doi.org/10.18632/aging.102700 pp 1563—1576

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Tao Y, Li R, Shen C, Li J, Zhang Q, Ma Z, Wang F, Wang Z, . SENP1 is a crucial promotor for hepatocellular carcinoma through deSUMOylation of UBE2T. . 12:1563-1576. https://doi.org/10.18632/aging.102700

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                TY  - JOUR
                AU  - Tao, Yifeng 
                AU  - Li, Ruidong 
                AU  - Shen, Conghuan 
                AU  - Li, Jianhua 
                AU  - Zhang, Quanbao 
                AU  - Ma, Zhenyu 
                AU  - Wang, Feifei 
                AU  - Wang, Zhengxin 
                TI  - SENP1 is a crucial promotor for hepatocellular carcinoma through deSUMOylation of UBE2T
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102700
                DO  - 10.18632/aging.102700
                SP  - 1563
                EP  - 1576
                PY  - 
                AB  - The cooperative roles of SENP1 and UBE2T in development and progression of hepatocellular carcinoma (HCC) are still unknown. The expression levels of SENP1 and UBE2T were evaluated in clinical specimens and HCC cells. The relationship between clinicopathological features and SENP1 were analyzed. We constructed the HepG2-SENP1 knockout cell model and explored the functions of SENP1 and UBE2T in HCC development. UBE2T was confirmed as a novel deSUMOylation target of SENP1. Upregulation of SENP1 and UBE2T were observed in HCC tissues and most hepatoma cell lines, and their expression levels were proved to be positively related. Knockout of SENP1 resulted in impaired growth, migration and invasion, and enhanced apoptosis in vitro, as well as inhibition of tumor growth in vivo. Furthermore, we demonstrated that SENP1 could directly deSUMOylate UBE2T thereby increasing its expression and activating Akt pathway. Functional studies showed that UBE2T overexpression or K8R mutation promoted cell growth, migration and invasion. In conclusion, our study demonstrated that SENP1 and UBE2T were positively related and functioned as tumor promoters. The carcinogenesis of SENP1 is mediated by deSUMOylation of UBE2T and the UBE2T/Akt pathway. Notably, UBE2T was identified as a novel deSUMOylation target of SENP1 in this study for the first time.
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PIK3CA gene mutations in the helical domain correlate with high tumor mutation burden and poor prognosis in metastatic breast carcinomas with late-line therapies

Yu Tang, Jing Li, Ning Xie, Xiaohong Yang, Liping Liu, Hui Wu, Can Tian, Ying He, Xiao Wang, Qiongzhi He, Zhe-Yu Hu, Quchang Ouyang,

https://doi.org/10.18632/aging.102701 pp 1577—1590

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Tang Y, Li J, Xie N, Yang X, Liu L, Wu H, Tian C, He Y, Wang X, He Q, Hu Z, Ouyang Q, . PIK3CA gene mutations in the helical domain correlate with high tumor mutation burden and poor prognosis in metastatic breast carcinomas with late-line therapies. . 12:1577-1590. https://doi.org/10.18632/aging.102701

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Provider: 
 TY - JOUR
 AU - Tang, Yu 
 AU - Li, Jing 
 AU - Xie, Ning 
 AU - Yang, Xiaohong 
 AU - Liu, Liping 
 AU - Wu, Hui 
 AU - Tian, Can 
 AU - He, Ying 
 AU - Wang, Xiao 
 AU - He, Qiongzhi 
 AU - Hu, Zhe-Yu 
 AU - Ouyang, Quchang 
 TI - PIK3CA gene mutations in the helical domain correlate with high tumor mutation burden and poor prognosis in metastatic breast carcinomas with late-line therapies
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102701
 DO - 10.18632/aging.102701
 SP - 1577
 EP - 1590
 PY - 
 AB - Nearly half of metastatic breast cancers (MBC) have genetic aberrations in the PI3K/AKT pathway. To investigate the distinct effect of these aberrations on MBC, 193 MBC patients who progressed after the early line (&#x2264;2) salvage treatment voluntarily received next generation sequencing (NGS) for a panel of 1,021 genes. 93 (48%) patients had genetic aberrations in the PI3K/AKT pathway. The number of patients with PIK3CA mutations in kinase domain (KD), helical domain (HD) and other domain (OD), were 36 (18.7%), 26 (13.5%), 10 (5.2%), respectively. 21 (10.9%) patients had mutations in PI3K/AKT pathway genes other than PIK3CA (P/A). Compared to PI3K/AKT-wild type (WT) patients, PIK3CA-HD patients had a significantly shorter progression-free survival (PFS) (Logrank p-value &lt; 0.0001). PIK3CA-KD, PIK3CA-OD and other P/A mutations showed similar PFS to WT patients (Logrank p-value = 0.63). PIK3CA-HD patients had a distinct ctDNA mutation profile to patients with other PI3K/AKT mutations. PIK3CA-HD patients had a higher rate of FGFR and NF1 aberrations. In addition, more PIK3CA-HD carriers were TMB-high. Cox regression analyses suggested that PIK3CA-HD mutations, FGFR aberrations and high TMB were all significant risk factors for poor PFS. In conclusion, future research needs to focus more on the treatment strategies targeting PIK3CA-HD mutations.
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Chikusetsu saponin IVa protects pancreatic β cell against intermittent high glucose-induced injury by activating Wnt/β-catenin/TCF7L2 pathway

Jia Cui, Jialin Duan, Jianjie Chu, Chao Guo, Miaomiao Xi, Yi Li, Yan Weng, Guo Wei, Ying Yin, Aidong Wen, Boling Qiao,

https://doi.org/10.18632/aging.102702 pp 1591—1609

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Cui J, Duan J, Chu J, Guo C, Xi M, Li Y, Weng Y, Wei G, Yin Y, Wen A, Qiao B, . Chikusetsu saponin IVa protects pancreatic β cell against intermittent high glucose-induced injury by activating Wnt/β-catenin/TCF7L2 pathway. . 12:1591-1609. https://doi.org/10.18632/aging.102702

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                TY  - JOUR
                AU  - Cui, Jia 
                AU  - Duan, Jialin 
                AU  - Chu, Jianjie 
                AU  - Guo, Chao 
                AU  - Xi, Miaomiao 
                AU  - Li, Yi 
                AU  - Weng, Yan 
                AU  - Wei, Guo 
                AU  - Yin, Ying 
                AU  - Wen, Aidong 
                AU  - Qiao, Boling 
                TI  - Chikusetsu saponin IVa protects pancreatic β cell against intermittent high glucose-induced injury by activating Wnt/β-catenin/TCF7L2 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102702
                DO  - 10.18632/aging.102702
                SP  - 1591
                EP  - 1609
                PY  - 
                AB  - Islet &#x3B2; cell mass reduction induced by glucose fluctuation is crucial for the development and progression of T2DM. Chikusetsu saponin IVa (CHS) had protective effects against DM and related injuries. Here we aimed to investigate the role of CHS in &#x3B2; cell injuries and its possible mechanism involved. Isolated rat islets, &#x3B2;TC3 cells and T2DM mice were used in this study. The results showed that CHS restored the secretion activity, promoted &#x3B2; cell survival by increasing &#x3B2; cell proliferation and decreasing apoptosis which induced by intermittent high glucose (IHG). In vivo, CHS protected &#x3B2; cell apoptosis to normalize blood glucose and improve insulin sensitivity in DM mice. Further studies showed that CHS activated Wnt3a signaling, inhibited HBP1, promoted &#x3B2;-catenin nuclear translocation, enhanced expressions of TCF7L2, GIPR and GLP-1R, inhibited p53, p27 and p21. The protective effect of CHS was remarkably suppressed by siRNAs against TCF7L2 or XAV-939 (a Wnt/&#x3B2;-catenin antagonist) in vitro and in &#x3B2;-catenin-/- mice. In conclusion, we identified a novel role of CHS in protecting &#x3B2; cell survival and regeneration by mechanisms involving the activation of Wnt3a/&#x3B2;-catenin/TCF7L2 signaling. Our results indicated the potential value of CHS as a possible intervention drug for T2DM.
                ER  -

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Melatonin ameliorates the advanced maternal age-associated meiotic defects in oocytes through the SIRT2-dependent H4K16 deacetylation pathway

Congyang Li, Xi He, Zhenyue Huang, Longsen Han, Xinghan Wu, Ling Li, Yongan Xin, Juan Ge, Jiahao Sha, Zhiqiang Yin, Qiang Wang,

https://doi.org/10.18632/aging.102703 pp 1610—1623

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Li C, He X, Huang Z, Han L, Wu X, Li L, Xin Y, Ge J, Sha J, Yin Z, Wang Q, . Melatonin ameliorates the advanced maternal age-associated meiotic defects in oocytes through the SIRT2-dependent H4K16 deacetylation pathway. . 12:1610-1623. https://doi.org/10.18632/aging.102703

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                TY  - JOUR
                AU  - Li, Congyang 
                AU  - He, Xi 
                AU  - Huang, Zhenyue 
                AU  - Han, Longsen 
                AU  - Wu, Xinghan 
                AU  - Li, Ling 
                AU  - Xin, Yongan 
                AU  - Ge, Juan 
                AU  - Sha, Jiahao 
                AU  - Yin, Zhiqiang 
                AU  - Wang, Qiang 
                TI  - Melatonin ameliorates the advanced maternal age-associated meiotic defects in oocytes through the SIRT2-dependent H4K16 deacetylation pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102703
                DO  - 10.18632/aging.102703
                SP  - 1610
                EP  - 1623
                PY  - 
                AB  - It has been widely reported that advanced maternal age impairs oocyte quality. To date, various molecules have been discovered to be involved in this process. However, prevention of fertility issues associated with maternal age is still a challenge. In the present study, we find that both in vitro supplement and in vivo administration of melatonin are capable of alleviating the meiotic phenotypes of aged oocytes, specifically the spindle/chromosome disorganization and aneuploidy generation. Furthermore, we identify SIRT2 as a critical effector mediating the effects of melatonin on meiotic structure in old oocytes. Candidate screening shows that SIRT2-controlled deacetylation of histone H4K16 is essential for maintaining the meiotic apparatus in oocytes. Importantly, non-acetylatable-mimetic mutant H4K16R partially rescues the meiotic deficits in oocytes from reproductive aged mice. In contrast, overexpression of acetylation-mimetic mutant H4K16Q abolishes the beneficial effects of melatonin on the meiotic phenotypes in aged oocytes. To sum up, our data uncover that melatonin alleviates advanced maternal aged-associated meiotic defects in oocytes through the SIRT2-depenendet H4K16 deacetylation pathway.
                ER  -

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TPGS-1000 exhibits potent anticancer activity for hepatocellular carcinoma in vitro and in vivo

Yidan Chen, Liqin Mo, Xuan Wang, Bi Chen, Yunfen Hua, Linyan Gong, Fei Yang, Yongqiang Li, Fangfang Chen, Guiting Zhu, Wei Ni, Cheng Zhang, Yuming Cheng, Yan Luo, Junping Shi, Mengsheng Qiu, Shixiu Wu, Zhou Tan, Kaifeng Wang,

https://doi.org/10.18632/aging.102704 pp 1624—1642

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Chen Y, Mo L, Wang X, Chen B, Hua Y, Gong L, Yang F, Li Y, Chen F, Zhu G, Ni W, Zhang C, Cheng Y, et al, . TPGS-1000 exhibits potent anticancer activity for hepatocellular carcinoma in vitro and in vivo. . 12:1624-1642. https://doi.org/10.18632/aging.102704

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Provider: 
 TY - JOUR
 AU - Chen, Yidan 
 AU - Mo, Liqin 
 AU - Wang, Xuan 
 AU - Chen, Bi 
 AU - Hua, Yunfen 
 AU - Gong, Linyan 
 AU - Yang, Fei 
 AU - Li, Yongqiang 
 AU - Chen, Fangfang 
 AU - Zhu, Guiting 
 AU - Ni, Wei 
 AU - Zhang, Cheng 
 AU - Cheng, Yuming 
 AU - Luo, Yan 
 AU - Shi, Junping 
 AU - Qiu, Mengsheng 
 AU - Wu, Shixiu 
 AU - Tan, Zhou 
 AU - Wang, Kaifeng 
 TI - TPGS-1000 exhibits potent anticancer activity for hepatocellular carcinoma in vitro and in vivo
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102704
 DO - 10.18632/aging.102704
 SP - 1624
 EP - 1642
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Chen, Yidan 
 AU - Mo, Liqin 
 AU - Wang, Xuan 
 AU - Chen, Bi 
 AU - Hua, Yunfen 
 AU - Gong, Linyan 
 AU - Yang, Fei 
 AU - Li, Yongqiang 
 AU - Chen, Fangfang 
 AU - Zhu, Guiting 
 AU - Ni, Wei 
 AU - Zhang, Cheng 
 AU - Cheng, Yuming 
 AU - Luo, Yan 
 AU - Shi, Junping 
 AU - Qiu, Mengsheng 
 AU - Wu, Shixiu 
 AU - Tan, Zhou 
 AU - Wang, Kaifeng 
 TI - TPGS-1000 exhibits potent anticancer activity for hepatocellular carcinoma in vitro and in vivo
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102704
 DO - 10.18632/aging.102704
 SP - 1624
 EP - 1642
 PY - 
 AB - D-alpha-tocopheryl polyethylene glycol 1000 succinate (TPGS1000) is the most active water-soluble derivative of vitamin E and has been widely used as a carrier of solvents, plasticizers, emulsifiers, absorbent agents and refractory drug delivery systems. However, its anti-hepatocellular carcinoma (HCC) properties have not been explored. HCC cells were treated with different concentrations of TPGS1000. Cell survival was tested by CCK8 assay, and cell migration was tested by wound healing and Transwell assay. EdU staining verified cell proliferation, and signalling pathway was assayed by Western blot analysis. The BALB/c-nu mouse xenograft model was established to test HCC cell growth in vivo. In vitro TPGS1000 significantly inhibited the viability and mobility of HCC cells (HepG2, Hep3B and Huh7) in a dose-dependent manner. Cell cycle analysis indicated that TPGS1000 treatment arrested the HCC cell cycle in the G0/G1 phase, and induction of cell apoptosis was confirmed by TUNEL and Annexin V-7-AAD staining. Further pharmacological analysis indicated that collapse of the transmembrane potential of mitochondria, increased ROS generation, PARP-induced cell apoptosis and FoxM1-p21-mediated cell cycle arresting, were involved in the anti-HCC activity of TPGS1000. Moreover, treatment in vivo with TPGS1000 effectively impaired the growth of HCC xenografts in nude mice.
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Hsa_circ_0070963 inhibits liver fibrosis via regulation of miR-223-3p and LEMD3

Dong Ji, Guo-Feng Chen, Jin-Cheng Wang, Si-Han Ji, Xue-Wen Wu, Xiao-Jie Lu, Jin-Lian Chen, Jing-Tao Li,

https://doi.org/10.18632/aging.102705 pp 1643—1655

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Ji D, Chen G, Wang J, Ji S, Wu X, Lu X, Chen J, Li J, . Hsa_circ_0070963 inhibits liver fibrosis via regulation of miR-223-3p and LEMD3. . 12:1643-1655. https://doi.org/10.18632/aging.102705

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                TY  - JOUR
                AU  - Ji, Dong 
                AU  - Chen, Guo-Feng 
                AU  - Wang, Jin-Cheng 
                AU  - Ji, Si-Han 
                AU  - Wu, Xue-Wen 
                AU  - Lu, Xiao-Jie 
                AU  - Chen, Jin-Lian 
                AU  - Li, Jing-Tao 
                TI  - Hsa_circ_0070963 inhibits liver fibrosis via regulation of miR-223-3p and LEMD3
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102705
                DO  - 10.18632/aging.102705
                SP  - 1643
                EP  - 1655
                PY  - 
                AB  - Previous circular RNA (circRNA) microarray analyses have uncovered an abnormal expression of hsa_circ_0070963 in hepatic stellate cells (HSCs). However, the specific role of hsa_circ_0070963 in liver fibrosis remains unknown. Here, we show that hsa_circ_0070963 inhibits liver fibrosis via regulation of miR-223-3p and LEMD3. Moreover, we demonstrated that hsa_circ_0070963 levels were reduced during liver fibrosis while restoring hsa_circ_0070963 levels abolished HSC activation, with a reduction in &#x3B1;-SMA and type I collagen levels both in vitro and in vivo. Furthermore, hsa_circ_0070963 overexpression suppressed both cell proliferation and the cell cycle of HSCs. MiR-223-3p was confirmed as a target of hsa_circ_0070963 and was shown to be involved in the effects of hsa_circ_0070963 on HSC activation. Furthermore, LEMD3 was confirmed as a target of miR-223-3p and was shown to be responsible for the activation of HSCs. The interactions between hsa_circ_0070963, miR-223-3p, and LEMD3 were validated via bioinformatic analysis, luciferase reporter assays, and rescue experiments. Collectively, hsa_circ_0070963 appeared to function as a miR-223-3p sponge that inhibited HSC activation in liver fibrosis via regulation of miR-223-3p and LEMD3. Therefore, hsa_circ_0070963 may serve as a potential therapeutic target for liver fibrosis.
                ER  -

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Elevated lymphocyte specific protein 1 expression is involved in the regulation of leukocyte migration and immunosuppressive microenvironment in glioblastoma

Jing-Yuan Cao, Qing Guo, Ge-Fei Guan, Chen Zhu, Cun-Yi Zou, Lu-Yang Zhang, Wen Cheng, Guo-li Wang, Peng Cheng, An-Hua Wu, Guang-Yu Li,

https://doi.org/10.18632/aging.102706 pp 1656—1684

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Cao J, Guo Q, Guan G, Zhu C, Zou C, Zhang L, Cheng W, Wang G, Cheng P, Wu A, Li G, . Elevated lymphocyte specific protein 1 expression is involved in the regulation of leukocyte migration and immunosuppressive microenvironment in glioblastoma. . 12:1656-1684. https://doi.org/10.18632/aging.102706

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                TY  - JOUR
                AU  - Cao, Jing-Yuan 
                AU  - Guo, Qing 
                AU  - Guan, Ge-Fei 
                AU  - Zhu, Chen 
                AU  - Zou, Cun-Yi 
                AU  - Zhang, Lu-Yang 
                AU  - Cheng, Wen 
                AU  - Wang, Guo-li 
                AU  - Cheng, Peng 
                AU  - Wu, An-Hua 
                AU  - Li, Guang-Yu 
                TI  - Elevated lymphocyte specific protein 1 expression is involved in the regulation of leukocyte migration and immunosuppressive microenvironment in glioblastoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102706
                DO  - 10.18632/aging.102706
                SP  - 1656
                EP  - 1684
                PY  - 
                AB  - Immune cell infiltration mediates therapeutic response to immune therapies. The investigation on the genes regulating leukocyte migration may help us to understand the mechanisms regulating immune cell infiltration in tumor microenvironment. Here, we collected the data from Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA) to analyze the expression of leukocyte migration related genes in glioblastoma (GBM). Lymphocyte specific protein 1 (LSP1) was identified as the only gene in this family which not only has an elevated expression, but also serve as an independent predictive factor for progressive malignancy in glioma. We further confirmed these results in clinical glioma samples by quantitative PCR, immunofluorescence, immunohistochemistry, and western blot. Moreover, LSP1 expression was closely related to the response to radio- and chemotherapy in GBM, and positively correlated with immunosuppressive cell populations, including M2 macrophages, neutrophil, and regulatory T cell. Additionally, elevated LSP-1 expression enhanced the expression of immunosuppression related genes like programmed cell death 1 (PD1) and leukocyte associated immunoglobulin like receptor 1 (LAIR1) in macrophages. LSP1 also promoted the migration of macrophages. Together, our study suggests a novel role of LSP1 contributing to immunosuppressive microenvironment in GBM and serving as a potential therapeutic target for it.
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The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation

Lin Lin, Yang Li, Mingli Liu, Qingbin Li, Quan Liu, Ruiyan Li,

https://doi.org/10.18632/aging.102707 pp 1685—1703

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Lin L, Li Y, Liu M, Li Q, Liu Q, Li R, . The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation. . 12:1685-1703. https://doi.org/10.18632/aging.102707

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                TY  - JOUR
                AU  - Lin, Lin 
                AU  - Li, Yang 
                AU  - Liu, Mingli 
                AU  - Li, Qingbin 
                AU  - Liu, Quan 
                AU  - Li, Ruiyan 
                TI  - The Interleukin-33/ST2 axis promotes glioma mesenchymal transition, stemness and TMZ resistance via JNK activation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102707
                DO  - 10.18632/aging.102707
                SP  - 1685
                EP  - 1703
                PY  - 
                AB  - IL-33 is an important member of the IL-1 family which has pleiotropic activities in innate and adaptive immune responses. Recently, some researchers have focused on the function of cellular immunity in the development of tumor. The biological role of IL-33 in glioma is poorly understood. In this study, we showed that glioma cells and tissues expressed higher levels of IL-33 and its receptor ST2 compared to normal brain. Clinically, IL-33 expression was associated with poor survival in patients with glioma. Administration of human IL-33 enhanced cell migration, invasion, epithelial to mesenchymal transition and stemness. Anti-ST2 blocked these effects of IL-33 on tumor. Mechanistically, IL-33 activated JNK signaling pathway via ST2 and increased the expression of key transcription factors that controlled the process of EMT and stemness. Moreover, IL-33 prevented temozolomide induced tumor apoptosis. Anti-ST2 or knockdown IL-33 increased the sensitivity of tumor to temozolomide. Thus, targeting the IL-33/ST2 axis may offer an opportunity to the treatment of glioma patients.
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Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy

Yun Luo, Shan Lu, Ye Gao, Ke Yang, Daoshun Wu, Xudong Xu, Guibo Sun, Xiaobo Sun,

https://doi.org/10.18632/aging.102708 pp 1704—1724

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Luo Y, Lu S, Gao Y, Yang K, Wu D, Xu X, Sun G, Sun X, . Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy. . 12:1704-1724. https://doi.org/10.18632/aging.102708

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                TY  - JOUR
                AU  - Luo, Yun 
                AU  - Lu, Shan 
                AU  - Gao, Ye 
                AU  - Yang, Ke 
                AU  - Wu, Daoshun 
                AU  - Xu, Xudong 
                AU  - Sun, Guibo 
                AU  - Sun, Xiaobo 
                TI  - Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102708
                DO  - 10.18632/aging.102708
                SP  - 1704
                EP  - 1724
                PY  - 
                AB  - Atherosclerosis-related cardiovascular disease is still the predominant cause of death worldwide. Araloside C (AsC), a natural saponin, exerts extensive anti-inflammatory properties. In this study, we explored the protective effects and mechanism of AsC on macrophage polarization in atherosclerosis in vivo and in vitro. Using a high-fat diet (HFD)-fed ApoE-/- mouse model and RAW264.7 macrophages exposed to ox-LDL, AsC was evaluated for its effects on polarization and autophagy. AsC significantly reduced the plaque area in atherosclerotic mice and lipid accumulation in ox-LDL-treated macrophages, promoted M2 phenotype macrophage polarization, increased the number of autophagosomes and modulated the expression of autophagy-related proteins. Moreover, the autophagy inhibitor 3-methyladenine and BECN1 siRNA obviously abolished the antiatherosclerotic and M2 macrophage polarization effects of AsC. Mechanistically, AsC targeted Sirt1and increased its expression, and this increase in expression was associated with increased autophagy and M2 phenotype polarization. In contrast, the effects of AsC were markedly blocked by EX527 and Sirt1 siRNA. Altogether, AsC attenuates foam cell formation and lessens atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy.
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Female adipose tissue has improved adaptability and metabolic health compared to males in aged obesity

Mita Varghese, Cameron Griffin, Kaitlin McKernan, Leila Eter, Simin Abrishami, Kanakadurga Singer,

https://doi.org/10.18632/aging.102709 pp 1725—1746

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Varghese M, Griffin C, McKernan K, Eter L, Abrishami S, Singer K, . Female adipose tissue has improved adaptability and metabolic health compared to males in aged obesity. . 12:1725-1746. https://doi.org/10.18632/aging.102709

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                TY  - JOUR
                AU  - Varghese, Mita 
                AU  - Griffin, Cameron 
                AU  - McKernan, Kaitlin 
                AU  - Eter, Leila 
                AU  - Abrishami, Simin 
                AU  - Singer, Kanakadurga 
                TI  - Female adipose tissue has improved adaptability and metabolic health compared to males in aged obesity
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102709
                DO  - 10.18632/aging.102709
                SP  - 1725
                EP  - 1746
                PY  - 
                AB  - Aging, like obesity, is associated with metabolic and inflammatory alterations within adipose tissue in older individuals. Younger females are protected from adipose inflammation, but older post-menopausal females exhibit exaggerated visceral adiposity correlated with increased disease risk. Obesity accelerates the onset and progression of age-associated diseases, but it is unclear if aging and obesity drive adipose tissue dysfunction in a sexually dimorphic fashion. We investigated adipose tissue metabolism and inflammation in a diet-induced obesity model in young and old mice. We identified age related sex differences in adipose tissue macrophages (ATMs), fibrosis and lipid metabolism in male and female visceral fat depot (GWAT). Although aging normalized body weights between the sexes, females remained protected from proinflammatory ATMs and stimulated lipolysis failed to adversely affect the inflammatory state even with obesity. Older obese males had augmented CD11c+ ATMs and higher insulin levels, while females showed increased visceral adiposity and exaggerated Ppar&#x3B3;, and Pgc1&#x3B1; expression. Obesity in aging demonstrated similar expression of GWAT p53, p16, p21, Timp1 and Tgf&#x3B2;1 in both sexes. Our studies suggest that even with aging, female GWAT shows an attenuated inflammatory response compared to males due to an efficient oxidative metabolism combined with an active tissue remodeling state.
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K63 ubiquitin chains target NLRP3 inflammasome for autophagic degradation in ox-LDL-stimulated THP-1 macrophages

Zhenfeng Zhou, Xiaoyan Zhu, Ruihua Yin, Tianwei Liu, Shaonan Yang, Lingyan Zhou, Xudong Pan, Aijun Ma,

https://doi.org/10.18632/aging.102710 pp 1747—1759

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Zhou Z, Zhu X, Yin R, Liu T, Yang S, Zhou L, Pan X, Ma A, . K63 ubiquitin chains target NLRP3 inflammasome for autophagic degradation in ox-LDL-stimulated THP-1 macrophages. . 12:1747-1759. https://doi.org/10.18632/aging.102710

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                TY  - JOUR
                AU  - Zhou, Zhenfeng 
                AU  - Zhu, Xiaoyan 
                AU  - Yin, Ruihua 
                AU  - Liu, Tianwei 
                AU  - Yang, Shaonan 
                AU  - Zhou, Lingyan 
                AU  - Pan, Xudong 
                AU  - Ma, Aijun 
                TI  - K63 ubiquitin chains target NLRP3 inflammasome for autophagic degradation in ox-LDL-stimulated THP-1 macrophages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102710
                DO  - 10.18632/aging.102710
                SP  - 1747
                EP  - 1759
                PY  - 
                AB  - Inflammation, especially involving the NLRP3 inflammasome, is critical to atherosclerotic plaque formation. Enhanced autophagy can inhibit the development of atherosclerosis, and recent studies have revealed that NLRP3 inflammasome can be degraded by autophagy in atherosclerosis. In the present study, we established a foam-cell model to investigate the impact of oxidized low density lipoproteins (ox-LDLs) on autophagy and the inflammasome in atherosclerosis-related inflammation. We observed that ox-LDLs activated NLRP3 inflammasomes in macrophages and restricted autophagy in a time-and dose-dependent manner. We further observed through immunoprecipitation and siRNA knockdown that autophagic degradation of the NLRP3 inflammasome is dependent on K63 polyubiquitation of its NLRP3 subunit and subsequent binding by the adaptor protein p62. Our findings uncover a mechanism by which autophagy inhibits inflammation in atherosclerosis and the role of K63 in that process.
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Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats

Lifeng Jiang, Kai Xu, Jin Li, Xindie Zhou, Langhai Xu, Zhipeng Wu, Chiyuan Ma, Jisheng Ran, Pengfei Hu, Jiapeng Bao, Lidong Wu, Yan Xiong,

https://doi.org/10.18632/aging.102711 pp 1760—1777

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Jiang L, Xu K, Li J, Zhou X, Xu L, Wu Z, Ma C, Ran J, Hu P, Bao J, Wu L, Xiong Y, . Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats. . 12:1760-1777. https://doi.org/10.18632/aging.102711

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                TY  - JOUR
                AU  - Jiang, Lifeng 
                AU  - Xu, Kai 
                AU  - Li, Jin 
                AU  - Zhou, Xindie 
                AU  - Xu, Langhai 
                AU  - Wu, Zhipeng 
                AU  - Ma, Chiyuan 
                AU  - Ran, Jisheng 
                AU  - Hu, Pengfei 
                AU  - Bao, Jiapeng 
                AU  - Wu, Lidong 
                AU  - Xiong, Yan 
                TI  - Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102711
                DO  - 10.18632/aging.102711
                SP  - 1760
                EP  - 1777
                PY  - 
                AB  - Osteoarthritis (OA) is a chronic degenerative joint disease, related to the overexpression of matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), inflammation, and chondrocyte apoptosis. Nesfatin-1 is an adipokine, which plays an important role in the development of OA, especially in obese people. In the present study, cartilage degradation and apoptosis observed in OA patients was evaluated. Furthermore, the anti-inflammatory and anti-apoptotic effects of nesfatin-1, and its underlying in vitro and in vivo mechanisms were investigated. The results showed that nesfatin-1 increased significantly the expression of collagen type II alpha 1 chain (Col2a1), and reduced the expression of MMPs, ADAMTS5, cyclooxygenase (COX)-2, caspase-3, nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), interleukin (IL)-6, and chondrocyte apoptosis rate, which may be induced by IL-1&#x3B2; in rat chondrocytes. Furthermore, nesfatin-1 treatment prevented cartilage degeneration in the rat OA model. It was found that nesfatin-1 suppressed the IL-1&#x3B2;-induced activation of NF-&#x3BA;B, the mitogen-activated protein kinase (MAPK), and the Bax/Bcl-2 signal pathway in chondrocytes. These results suggest that in vivo nesfatin-1 could play a protective role in the development of OA and can be potentially used for its treatment.
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LncRNA DANCR attenuates brain microvascular endothelial cell damage induced by oxygen-glucose deprivation through regulating of miR-33a-5p/XBP1s

Mengqi Zhang, Mimi Tang, Qian Wu, Zhuolu Wang, Zhuohui Chen, Hui Ding, Xinhang Hu, Xinyi Lv, Songfeng Zhao, Jingyan Sun, Shuntong Kang, Tong Wu, Bo Xiao,

https://doi.org/10.18632/aging.102712 pp 1778—1791

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Zhang M, Tang M, Wu Q, Wang Z, Chen Z, Ding H, Hu X, Lv X, Zhao S, Sun J, Kang S, Wu T, Xiao B, . LncRNA DANCR attenuates brain microvascular endothelial cell damage induced by oxygen-glucose deprivation through regulating of miR-33a-5p/XBP1s. . 12:1778-1791. https://doi.org/10.18632/aging.102712

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                TY  - JOUR
                AU  - Zhang, Mengqi 
                AU  - Tang, Mimi 
                AU  - Wu, Qian 
                AU  - Wang, Zhuolu 
                AU  - Chen, Zhuohui 
                AU  - Ding, Hui 
                AU  - Hu, Xinhang 
                AU  - Lv, Xinyi 
                AU  - Zhao, Songfeng 
                AU  - Sun, Jingyan 
                AU  - Kang, Shuntong 
                AU  - Wu, Tong 
                AU  - Xiao, Bo 
                TI  - LncRNA DANCR attenuates brain microvascular endothelial cell damage induced by oxygen-glucose deprivation through regulating of miR-33a-5p/XBP1s
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102712
                DO  - 10.18632/aging.102712
                SP  - 1778
                EP  - 1791
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhang, Mengqi 
                AU  - Tang, Mimi 
                AU  - Wu, Qian 
                AU  - Wang, Zhuolu 
                AU  - Chen, Zhuohui 
                AU  - Ding, Hui 
                AU  - Hu, Xinhang 
                AU  - Lv, Xinyi 
                AU  - Zhao, Songfeng 
                AU  - Sun, Jingyan 
                AU  - Kang, Shuntong 
                AU  - Wu, Tong 
                AU  - Xiao, Bo 
                TI  - LncRNA DANCR attenuates brain microvascular endothelial cell damage induced by oxygen-glucose deprivation through regulating of miR-33a-5p/XBP1s
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102712
                DO  - 10.18632/aging.102712
                SP  - 1778
                EP  - 1791
                PY  - 
                AB  - Brain microvascular endothelial cell (BMEC) survival and angiogenesis after ischemic stroke has great significance for improving the prognosis of stroke. Abnormal variants of lncRNAs are closely associated with stroke. In this study, we examined the effects and molecular mechanisms of differentiation antagonizing non-protein coding RNA (DANCR) on apoptosis, migration, and angiogenesis of oxygen-glucose deprivation (OGD)-treated BMECs. We found that DANCR expression significantly increased at 2, 4, 6, 8, and 10 h after OGD. DANCR overexpression promoted cell viability, migration, and angiogenesis in OGD-treated BMECs. Additionally, we found that X-box binding protein l splicing (XBP1s) expression was positively correlated with DANCR expression. DANCR overexpression promoted XBP1s expression in OGD-treated BMECs. Silenced XBP1s reversed the effect of DANCR in OGD-treated BMECs. Furthermore, we found that microRNA (miR)-33a-5p bound to DANCR and the 3&apos;-UTR of XBP1. miR-33a-5p overexpression inhibited proliferation, migration, angiogenesis, and XBP1s expression in OGD-treated DANCR-overexpressing BMECs, reversing the protective effect of DANCR. Finally, we found that XBP1s expression promoted proliferation, migration, and angiogenesis, reversing the damaging effect of miR-33a-5p. In conclusion, DANCR enhanced survival and angiogenesis in OGD-treated BMECs through the miR-33a-5p/XBP1s axis.
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The neuroprotective effects of SIRT1 in mice carrying the APP/PS1 double-transgenic mutation and in SH-SY5Y cells over-expressing human APP670/671 may involve elevated levels of α7 nicotinic acetylcholine receptors

Kun Cao, Yang-Ting Dong, Jie Xiang, Yi Xu, Yi Li, Hui Song, Wen-Feng Yu, Xiao-Lan Qi, Zhi-Zhong Guan,

https://doi.org/10.18632/aging.102713 pp 1792—1807

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Cao K, Dong Y, Xiang J, Xu Y, Li Y, Song H, Yu W, Qi X, Guan Z, . The neuroprotective effects of SIRT1 in mice carrying the APP/PS1 double-transgenic mutation and in SH-SY5Y cells over-expressing human APP670/671 may involve elevated levels of α7 nicotinic acetylcholine receptors. . 12:1792-1807. https://doi.org/10.18632/aging.102713

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                TY  - JOUR
                AU  - Cao, Kun 
                AU  - Dong, Yang-Ting 
                AU  - Xiang, Jie 
                AU  - Xu, Yi 
                AU  - Li, Yi 
                AU  - Song, Hui 
                AU  - Yu, Wen-Feng 
                AU  - Qi, Xiao-Lan 
                AU  - Guan, Zhi-Zhong 
                TI  - The neuroprotective effects of SIRT1 in mice carrying the APP/PS1 double-transgenic mutation and in SH-SY5Y cells over-expressing human APP670/671 may involve elevated levels of α7 nicotinic acetylcholine receptors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102713
                DO  - 10.18632/aging.102713
                SP  - 1792
                EP  - 1807
                PY  - 
                AB  - The aim was to determine whether the neuroprotective effect of SIRT1 in Alzheimer&#x2019;s disease (AD), due to inhibition of aggregation of the &#x3B2;-amyloid peptide (A&#x3B2;), involves activation of &#x3B1;7 nAChR. In present study, four-month-old APP/PS1 mice were administered resveratrol (RSV) or suramin once daily for two months, following which their spatial learning and memory were assessed using the Morris water maze test. Deposits of A&#x3B2; in vivo were detected by near-infrared imaging (NIRI) and confocal laser scanning. SH-SY5Y/APPswe cells were treated with RSV, suramin, U0126 or methyllycaconitine (MLA). Levels of proteins and mRNA were determined by Western blotting and qRT-PCR, respectively. The results show that activation of SIRT1 improved their spatial learning and memory and reduced the production and aggregation of A&#x3B2; in the hippocampus and cerebral cortex; whereas inhibition of SIRT1 had the opposite effects. In addition, activation of SIRT1 increased the levels of both &#x3B1;7 nAChR and &#x3B1;APP in the brains these animals. Finally, activation of SIRT1 elevated the levels of pERK1/2, while inhibition of ERK1/2 counteracted the increase in &#x3B1;7 nAChR caused by RSV. These findings indicate that neuroprotection by SIRT1 may involve increasing levels of &#x3B1;7 nAChR through activation of the MAPK/ERK1/2 signaling pathway.
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ISG20 serves as a potential biomarker and drives tumor progression in clear cell renal cell carcinoma

Tianbo Xu, Hailong Ruan, Su Gao, Jingchong Liu, Yuenan Liu, Zhengshuai Song, Qi Cao, Keshan Wang, Lin Bao, Di Liu, Junwei Tong, Jian Shi, Huageng Liang, Hongmei Yang, Ke Chen, Xiaoping Zhang,

https://doi.org/10.18632/aging.102714 pp 1808—1827

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Xu T, Ruan H, Gao S, Liu J, Liu Y, Song Z, Cao Q, Wang K, Bao L, Liu D, Tong J, Shi J, Liang H, et al, . ISG20 serves as a potential biomarker and drives tumor progression in clear cell renal cell carcinoma. . 12:1808-1827. https://doi.org/10.18632/aging.102714

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                TY  - JOUR
                AU  - Xu, Tianbo 
                AU  - Ruan, Hailong 
                AU  - Gao, Su 
                AU  - Liu, Jingchong 
                AU  - Liu, Yuenan 
                AU  - Song, Zhengshuai 
                AU  - Cao, Qi 
                AU  - Wang, Keshan 
                AU  - Bao, Lin 
                AU  - Liu, Di 
                AU  - Tong, Junwei 
                AU  - Shi, Jian 
                AU  - Liang, Huageng 
                AU  - Yang, Hongmei 
                AU  - Chen, Ke 
                AU  - Zhang, Xiaoping 
                TI  - ISG20 serves as a potential biomarker and drives tumor progression in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102714
                DO  - 10.18632/aging.102714
                SP  - 1808
                EP  - 1827
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Xu, Tianbo 
                AU  - Ruan, Hailong 
                AU  - Gao, Su 
                AU  - Liu, Jingchong 
                AU  - Liu, Yuenan 
                AU  - Song, Zhengshuai 
                AU  - Cao, Qi 
                AU  - Wang, Keshan 
                AU  - Bao, Lin 
                AU  - Liu, Di 
                AU  - Tong, Junwei 
                AU  - Shi, Jian 
                AU  - Liang, Huageng 
                AU  - Yang, Hongmei 
                AU  - Chen, Ke 
                AU  - Zhang, Xiaoping 
                TI  - ISG20 serves as a potential biomarker and drives tumor progression in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102714
                DO  - 10.18632/aging.102714
                SP  - 1808
                EP  - 1827
                PY  - 
                AB  - Clear cell renal cell carcinoma (ccRCC) is one of the most common malignancies and lacks reliable biomarkers for diagnosis and prognosis, which results in high incidence and mortality rates of ccRCC. In this study, ISG20, HJURP, and FOXM1 were identified as hub genes via weighted gene co-expression network analysis (WGCNA) and Cox regression analysis. Samples validation showed that only ISG20 was up-regulated in ccRCC. Therefore, ISG20 was selected for further study. High ISG20 expression was associated with poor overall survival and disease-free survival. Furthermore, the expression of ISG20 could effectively differentiate ccRCC from normal tissues and was positively correlated to clinical stages. Functional experiments proved that knockdown of ISG20 expression could obviously inhibit cell growth, migration, and invasion in ccRCC cells. To find the potential mechanisms of ISG20, gene set enrichment analysis (GSEA) was performed and revealed that high expression of ISG20 was significantly involved in metastasis and cell cycle pathways. In addition, we found that ISG20 could regulate the expression of MMP9 and CCND1. In conclusion, these findings suggested that ISG20 promoted cell proliferation and metastasis via regulating MMP9/CCND1 expression and might serve as a potential biomarker and therapeutic target in ccRCC.
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Autophagy-related gene P4HB: a novel diagnosis and prognosis marker for kidney renal clear cell carcinoma

Longxiang Xie, Huimin Li, Lu Zhang, Xiaoyu Ma, Yifang Dang, Jinshuai Guo, Jiahao Liu, Linna Ge, Fangmei Nan, Huan Dong, Zhongyi Yan, Xiangqian Guo,

https://doi.org/10.18632/aging.102715 pp 1828—1842

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Xie L, Li H, Zhang L, Ma X, Dang Y, Guo J, Liu J, Ge L, Nan F, Dong H, Yan Z, Guo X, . Autophagy-related gene P4HB: a novel diagnosis and prognosis marker for kidney renal clear cell carcinoma. . 12:1828-1842. https://doi.org/10.18632/aging.102715

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Provider: 
 TY - JOUR
 AU - Xie, Longxiang 
 AU - Li, Huimin 
 AU - Zhang, Lu 
 AU - Ma, Xiaoyu 
 AU - Dang, Yifang 
 AU - Guo, Jinshuai 
 AU - Liu, Jiahao 
 AU - Ge, Linna 
 AU - Nan, Fangmei 
 AU - Dong, Huan 
 AU - Yan, Zhongyi 
 AU - Guo, Xiangqian 
 TI - Autophagy-related gene P4HB: a novel diagnosis and prognosis marker for kidney renal clear cell carcinoma
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102715
 DO - 10.18632/aging.102715
 SP - 1828
 EP - 1842
 PY - 
 AB - Autophagy can protect cells and organisms from stressors such as nutrient deprivation, and is involved in many pathological processes including human cancer. Therefore, it is necessary to investigate the role of autophagy-related genes (ARGs) in cancer. In this study, we investigated the gene expression of 222 ARGs in 1048 Kidney Renal Clear Cell Carcinoma (KIRC) cases, from 5 independent cohorts. The gene expression of ARGs were first evaluated in the The Cancer Genome Atlas (TCGA) by Recevier Operating Characteristic (ROC) analysis to select potential biomarkers with extremely high ability in KIRC detection (AUC&#x2265;0.85 and p&lt;0.0001). Then in silico procedure progressively leads to the selection of two genes in a three rounds of validation performed in four human KIRC-patients datasets including two independent Gene Expression Omnibus (GEO) datasets, Oncomine dataset and Human Protein Atlas dataset. Finally, only P4HB (Prolyl 4-hydroxylase, beta polypeptide) gene was experimentally validated by RT-PCR between control kidney cells and cancer cells. Following univariate and multivariate analyses of TCGA-KIRC clinical data showed that P4HB expression is an independent prognostic indicator of unfavorable overall survival (OS) for KIRC patients. Based on these findings, we proposed that P4HB might be one potential novel KIRC diagnostic and prognostic biomarker at both mRNA and protein levels.
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Long non-coding RNA PSMA3-AS1 promotes malignant phenotypes of esophageal cancer by modulating the miR-101/EZH2 axis as a ceRNA

Bai-Quan Qiu, Xia-Hui Lin, Xu-Dong Ye, Wei Huang, Xu Pei, Dian Xiong, Xiang Long, Shu-Qiang Zhu, Feng Lu, Kun Lin, Xiao-Qiang Zhang, Jian-Jun Xu, Lu-Lu Sheng, Xue-Mei Zhang, Peng-Fei Zhang, Yong-Bing Wu,

https://doi.org/10.18632/aging.102716 pp 1843—1856

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Qiu B, Lin X, Ye X, Huang W, Pei X, Xiong D, Long X, Zhu S, Lu F, Lin K, Zhang X, Xu J, Sheng L, et al, . Long non-coding RNA PSMA3-AS1 promotes malignant phenotypes of esophageal cancer by modulating the miR-101/EZH2 axis as a ceRNA. . 12:1843-1856. https://doi.org/10.18632/aging.102716

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                TY  - JOUR
                AU  - Qiu, Bai-Quan 
                AU  - Lin, Xia-Hui 
                AU  - Ye, Xu-Dong 
                AU  - Huang, Wei 
                AU  - Pei, Xu 
                AU  - Xiong, Dian 
                AU  - Long, Xiang 
                AU  - Zhu, Shu-Qiang 
                AU  - Lu, Feng 
                AU  - Lin, Kun 
                AU  - Zhang, Xiao-Qiang 
                AU  - Xu, Jian-Jun 
                AU  - Sheng, Lu-Lu 
                AU  - Zhang, Xue-Mei 
                AU  - Zhang, Peng-Fei 
                AU  - Wu, Yong-Bing 
                TI  - Long non-coding RNA PSMA3-AS1 promotes malignant phenotypes of esophageal cancer by modulating the miR-101/EZH2 axis as a ceRNA
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102716
                DO  - 10.18632/aging.102716
                SP  - 1843
                EP  - 1856
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Qiu, Bai-Quan 
                AU  - Lin, Xia-Hui 
                AU  - Ye, Xu-Dong 
                AU  - Huang, Wei 
                AU  - Pei, Xu 
                AU  - Xiong, Dian 
                AU  - Long, Xiang 
                AU  - Zhu, Shu-Qiang 
                AU  - Lu, Feng 
                AU  - Lin, Kun 
                AU  - Zhang, Xiao-Qiang 
                AU  - Xu, Jian-Jun 
                AU  - Sheng, Lu-Lu 
                AU  - Zhang, Xue-Mei 
                AU  - Zhang, Peng-Fei 
                AU  - Wu, Yong-Bing 
                TI  - Long non-coding RNA PSMA3-AS1 promotes malignant phenotypes of esophageal cancer by modulating the miR-101/EZH2 axis as a ceRNA
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102716
                DO  - 10.18632/aging.102716
                SP  - 1843
                EP  - 1856
                PY  - 
                AB  - Backgrounds: Emerging evidences has demonstrated that dysregulation of long non-coding RNAs (lncRNAs) is critically involved in esophageal squamous cell carcinoma (ESCC) progression. However, the function of lncRNA PSMA3-AS1 in ESCC is unclear. Therefore, we aimed to explore the functions and potential mechanisms of PSMA3-AS1 in ESCC cells progression.Results: Here, we found that PSMA3-AS1 expression was significantly up-regulated in ESCC tissues. Forced PSMA3-AS1 expression was correlated with tumor size, distant metastasis, and poor prognosis in ESCC patients. Functionally, PSMA3-AS1-overexpression promoted ESCC cells proliferation, invasion, and migration in vitro. Mechanistically, PSMA3-AS1 up-regulated EZH2 expression by competitively binding to miR-101.Conclusion: PSMA3-AS1 is significantly up-regulated in ESCC tissues, and the PSMA3-AS1/miR-101/EZH2 axis plays a critical role in ESCC progression. Taken together, our results may provide promising targets for ESCC therapy.Methods: PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines. Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression. RIP, dual-luciferase reporter, fluorescence in situ hybridization, and biotin pull-down assays were used to detect the interactions of PSMA3-AS1, miR-101 and EZH2. The biological functions of PSMA3-AS1 in PSMA3-AS1-altered cells were explored using CCK-8, colony formation, wound healing, and transwell assays in vitro.
                ER  -

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Prognostic nomogram of xerostomia for patients with nasopharyngeal carcinoma after intensity-modulated radiotherapy

Xin-Bin Pan, Yang Liu, Ling Li, Song Qu, Long Chen, Shi-Xiong Liang, Kai-Hua Chen, Zhong-Guo Liang, Xiao-Dong Zhu,

https://doi.org/10.18632/aging.102717 pp 1857—1866

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Pan X, Liu Y, Li L, Qu S, Chen L, Liang S, Chen K, Liang Z, Zhu X, . Prognostic nomogram of xerostomia for patients with nasopharyngeal carcinoma after intensity-modulated radiotherapy. . 12:1857-1866. https://doi.org/10.18632/aging.102717

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Provider: 
                TY  - JOUR
                AU  - Pan, Xin-Bin 
                AU  - Liu, Yang 
                AU  - Li, Ling 
                AU  - Qu, Song 
                AU  - Chen, Long 
                AU  - Liang, Shi-Xiong 
                AU  - Chen, Kai-Hua 
                AU  - Liang, Zhong-Guo 
                AU  - Zhu, Xiao-Dong 
                TI  - Prognostic nomogram of xerostomia for patients with nasopharyngeal carcinoma after intensity-modulated radiotherapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102717
                DO  - 10.18632/aging.102717
                SP  - 1857
                EP  - 1866
                PY  - 
                AB  - Xerostomia is a common radiation-induced late complication after radiotherapy. Identifying predictive factors for xerostomia will lead to better treatments and improve the quality of life. This study was conducted to establish an effective predictive nomogram for xerostomia by assessing stage I-IVb (AJCC 7th edition) NPC patients between September 2015 and March 2016. Xerostomia was evaluated via the RTOG/EORTC system. The primary endpoint was grade 2-3 xerostomia 1 year after treatment. The predictive factors for xerostomia were analysed using logistic regression analysis. A nomogram was constructed based on combining the predictors and clinical variables. In total, 102 patients with grade 0-1 xerostomia and 93 patients with grade 2-3 xerostomia were included. The independent predictive factors for xerostomia were V25, V30, V35, and V45 of the ipsilateral parotid gland and mean dose of the contralateral parotid gland. The calibration plot for the probability of xerostomia showed good agreement between prediction by the nomogram and actual observation. The concordance index of the nomogram for predicting xerostomia was 0.796 (95% CI: 0.735-0.857, P &lt;0.001), which was higher than any single dosimetric parameter. Our results indicated that the nomogram provided a more accurate prediction of grade 2-3 xerostomia 1 year after treatment.
                ER  -

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miR-106b-5p contributes to the lung metastasis of breast cancer via targeting CNN1 and regulating Rho/ROCK1 pathway

Zheng Wang, Tian-En Li, Mo Chen, Jun-Jie Pan, Kun-Wei Shen,

https://doi.org/10.18632/aging.102719 pp 1867—1887

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Wang Z, Li T, Chen M, Pan J, Shen K, . miR-106b-5p contributes to the lung metastasis of breast cancer via targeting CNN1 and regulating Rho/ROCK1 pathway. . 12:1867-1887. https://doi.org/10.18632/aging.102719

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Provider: 
                TY  - JOUR
                AU  - Wang, Zheng 
                AU  - Li, Tian-En 
                AU  - Chen, Mo 
                AU  - Pan, Jun-Jie 
                AU  - Shen, Kun-Wei 
                TI  - miR-106b-5p contributes to the lung metastasis of breast cancer via targeting CNN1 and regulating Rho/ROCK1 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102719
                DO  - 10.18632/aging.102719
                SP  - 1867
                EP  - 1887
                PY  - 
                AB  - Objectives: Breast cancer has been the second most prevalent and fatal malignancy due to its frequent metastasis to other organs. We aim to study the effects of a key miRNA-mRNA signaling in breast cancer.Results: CNN1 was identified as the key gene in breast cancer by the bioinformatics analysis, and the downregulation of CNN1 in breast cancer tissues and cell lines was observed. Upregulating CNN1 inhibited cell survival, migration, invasion, and adhesion, but enhanced cell apoptosis. miR-106b-5p not only bound to CNN1 mRNA 3&#x2019;UTR, but also promoted lung metastasis in vivo. Besides, the miR-106b-5p mimic enhanced breast cancer canceration by targeting CNN1 and activating Rho/ROCK1 signaling pathway.Conclusion: Overall, our results proved that miR-106b-5p promoted the metastasis of breast cancer by suppressing CNN1 and activating Rho/ROCK1 pathway.Methods: Bioinformatics analysis was performed to select the key gene in breast cancer. The overexpression and knockdown of Calponin 1 (CNN1) in breast cancer cell lines were performed to conduct cell viability, migrating, invasion, proliferation, adhesion, and apoptosis experiments. To identify the role of miR-106b-5p and Rho/ROCK1 in CNN1-induced breast cancer, a dual-luciferase assay, tumor lung metastasis assay, transcript half-life assay, and Rho/ROCK1 inhibition assay were performed.
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Clinical outcome of transurethral enucleation of the prostate using the 120-W thulium Laser (Vela™ XL) compared to bipolar transurethral resection of the prostate (TURP) in aging male

Chen-Pang Hou, Yu-Hsiang Lin, Horng-Heng Juang, Phei-Lang Chang, Chien-lun Chen, Pei-Shan Yang, Ke-Hung Tsui,

https://doi.org/10.18632/aging.102720 pp 1888—1898

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Hou C, Lin Y, Juang H, Chang P, Chen C, Yang P, Tsui K, . Clinical outcome of transurethral enucleation of the prostate using the 120-W thulium Laser (Vela™ XL) compared to bipolar transurethral resection of the prostate (TURP) in aging male. . 12:1888-1898. https://doi.org/10.18632/aging.102720

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                TY  - JOUR
                AU  - Hou, Chen-Pang 
                AU  - Lin, Yu-Hsiang 
                AU  - Juang, Horng-Heng 
                AU  - Chang, Phei-Lang 
                AU  - Chen, Chien-lun 
                AU  - Yang, Pei-Shan 
                AU  - Tsui, Ke-Hung 
                TI  - Clinical outcome of transurethral enucleation of the prostate using the 120-W thulium Laser (Vela™ XL) compared to bipolar transurethral resection of the prostate (TURP) in aging male
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102720
                DO  - 10.18632/aging.102720
                SP  - 1888
                EP  - 1898
                PY  - 
                AB  - This study compared the surgical outcomes of the 120-W Thulium laser (Vela&#x2122; XL) enucleation of the prostate and bipolar transurethral resection of the prostate (TURP) in terms of efficacy, safety, and improvements of quality of life (QoL) in patients with benign prostate hyperplasia (BPH). Records were obtained from January 2014 to September 2018 for selected patients with symptomatic BPH who underwent 120-W Thulium laser (Vela&#x2122;XL) prostate enucleation and bipolar TURP in our institution. All the patients selected met the surgical criteria for TURP and had received medical treatment for at least 3 months. Patients were excluded if their ECOG performance status was &gt;1, if they had active malignant disease, of if they had a history of prostate surgery or reconstruction surgery of the urinary system. Patients decided which treatment option would be performed. Both the procedures were conducted by a single surgeon. Clinical outcomes such as changes in the International Prostate Symptom Score (IPSS) score, urodynamic parameters, drug consumption, pain scores, and QoL were evaluated. The rate of urinary tract infection, recatheterization, additional analgesic requirement, return to the emergency department for treatment, and other surgical complications was analyzed and compared between the two cohorts. A total of 276 patients met the inclusion criteria. Among them, 141 patients received bipolar TURP, where as 135 decided to receive laser vaporesection. No significant difference was observed in age, PSA level, prostate volume, and comorbidities between the two cohorts. Pre-operative (pre-op) urodynamic parameters were also identical, except that the laser surgery group had a higher rate of admission with a urinary catheter (24.4% vs. 14.2%, p=0.044). The operating time was longer in the laser surgery group (79.3 minutes vs. 62.4 minutes, p&lt;0.001). However, enucleation using the Thulium laser was superior to bipolar TURP in terms of post-operative (post-op) pain status, including the numeric rating scale of pain, rate of additional narcotic use, and oral analgesic requirement. Compared with bipolar TURP, laser enucleation achieved a higher improvement in the QoL score at post-op follow-up at 2 weeks and 3 months. Nevertheless, the complication rate, changes in IPSS score, Qmax, and post-op medication-free survival were statistically identical in the two cohorts. Our data revealed that compared with bipolar TURP, 120-W Thulium laser (Vela&#x2122; XL) enucleation of the prostate achieved lower post-op pain and higher improvement in the short-term QoL of patients after surgery.
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Inhibition of miR-193a-3p protects human umbilical vein endothelial cells against intermittent hypoxia-induced endothelial injury by targeting FAIM2

Qingshi Chen, Guofu Lin, Jianchai Huang, Lida Chen, Yibin Liu, Jiefeng Huang, Shuyi Zhang, Qichang Lin,

https://doi.org/10.18632/aging.102729 pp 1899—1909

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Chen Q, Lin G, Huang J, Chen L, Liu Y, Huang J, Zhang S, Lin Q, . Inhibition of miR-193a-3p protects human umbilical vein endothelial cells against intermittent hypoxia-induced endothelial injury by targeting FAIM2. . 12:1899-1909. https://doi.org/10.18632/aging.102729

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Provider: 
 TY - JOUR
 AU - Chen, Qingshi 
 AU - Lin, Guofu 
 AU - Huang, Jianchai 
 AU - Chen, Lida 
 AU - Liu, Yibin 
 AU - Huang, Jiefeng 
 AU - Zhang, Shuyi 
 AU - Lin, Qichang 
 TI - Inhibition of miR-193a-3p protects human umbilical vein endothelial cells against intermittent hypoxia-induced endothelial injury by targeting FAIM2
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102729
 DO - 10.18632/aging.102729
 SP - 1899
 EP - 1909
 PY - 
 AB - Objective: The functions and molecular regulatory mechanisms of miR-193a-3p in cardiac injury induced by obstructive sleep apnea (OSA) are poorly understood. This study aimed to explore the role of miR-193a-3p in intermittent hypoxia(IH)-induced human umbilical vein endothelial cells (HUVECs) injury.Results: In this study, we found that IH significantly decreased viability but enhanced cell apoptosis. Concurrently, the miR-193a-3p expression level was increased in HUVECs after IH. Subsequent experiments showed that IH-induced injury was ameliorated through miR-193a-3p silence. Fas apoptotic inhibitory molecule 2 (FAIM2) was predicted by bioinformatics analysis and further identified as a direct target gene of miR-193a-3p. Interestingly, the effect of miR-193a-3p inhibition under IH could be reversed by down-regulating FAIM2 expression.Conclusion: In conclusion, our study first revealed that miR-193a-3p inhibition could protect HUVECs against intermittent hypoxia-induced damage by negatively regulating FAIM2. These findings could advance our understanding of the underlying mechanisms for OSA-related cardiac injury.Methods: We exposed HUVECs to IH condition; the expression levels of miR-193a-3p were detected by RT-qPCR. Cell viability, and the expressions of apoptosis-associated proteins were examined via CCK-8, and western blotting, respectively. Target genes of miR-193a-3p were confirmed by dual-luciferase reporter assay.
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Effect of antioxidants on the H₂O₂-induced premature senescence of human fibroblasts

Natalia Pieńkowska, Grzegorz Bartosz, Monika Pichla, Michalina Grzesik-Pietrasiewicz, Martyna Gruchala, Izabela Sadowska-Bartosz,

https://doi.org/10.18632/aging.102730 pp 1910—1927

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Pieńkowska N, Bartosz G, Pichla M, Grzesik-Pietrasiewicz M, Gruchala M, Sadowska-Bartosz I, . Effect of antioxidants on the H₂O₂-induced premature senescence of human fibroblasts. . 12:1910-1927. https://doi.org/10.18632/aging.102730

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Provider: 
 TY - JOUR
 AU - Pieńkowska, Natalia 
 AU - Bartosz, Grzegorz 
 AU - Pichla, Monika 
 AU - Grzesik-Pietrasiewicz, Michalina 
 AU - Gruchala, Martyna 
 AU - Sadowska-Bartosz, Izabela 
 TI - Effect of antioxidants on the H2O2-induced premature senescence of human fibroblasts
 JO - 
 JA - 
 VL - 12
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102730
 DO - 10.18632/aging.102730
 SP - 1910
 EP - 1927
 PY - 
 AB - The study was aimed at evaluation of the role of secondary oxidative stress in the stress-induced premature senescence (SIPS) of human fibroblasts induced by H2O2. Two fibroblast lines were used: lung MRC-5 and ear H8F2p25LM fibroblasts. The lines differed considerably in sensitivity to H2O2 (IC50 of 528 and 33.5 &#x3BC;M, respectively). The cells were exposed to H2O2 concentrations corresponding to IC50 and after 24 h supplemented with a range of antioxidants. Most of antioxidants studied slightly augmented the survival of fibroblasts at single concentrations or in a narrow concentration range, but the results were not consistent among the cell lines. Chosen antioxidants (4-amino-TEMPO, curcumin, caffeic acid and p-coumaric acid) did not restore the level of glutathione decreased by H2O2. Hydrogen peroxide treatment did not induce secondary production of H2O2 and even decreased it, decreased mitochondrial potential in both cell lines and induced changes in the mitochondrial mass inconsistent between the lines. Antioxidant protected mitochondrial potential only in H8F2p25LM cells, but attenuated changes in mitochondrial mass. These results speak against the intermediacy of secondary oxidative stress in the SIPS induced by H2O2 and suggest that the small protective action of antioxidants is due to their effects on mitochondria.
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Autocrine CXCL8-dependent invasiveness triggers modulation of actin cytoskeletal network and cell dynamics

Andrea Antonosante, Laura Brandolini, Michele d’Angelo, Elisabetta Benedetti, Vanessa Castelli, Mattia Del Maestro, Sabino Luzzi, Antonio Giordano, Annamaria Cimini, Marcello Allegretti,

https://doi.org/10.18632/aging.102733 pp 1928—1951

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Antonosante A, Brandolini L, d’Angelo M, Benedetti E, Castelli V, Maestro MD, Luzzi S, Giordano A, Cimini A, Allegretti M, . Autocrine CXCL8-dependent invasiveness triggers modulation of actin cytoskeletal network and cell dynamics. . 12:1928-1951. https://doi.org/10.18632/aging.102733

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                TY  - JOUR
                AU  - Antonosante, Andrea 
                AU  - Brandolini, Laura 
                AU  - d’Angelo, Michele 
                AU  - Benedetti, Elisabetta 
                AU  - Castelli, Vanessa 
                AU  - Maestro, Mattia Del 
                AU  - Luzzi, Sabino 
                AU  - Giordano, Antonio 
                AU  - Cimini, Annamaria 
                AU  - Allegretti, Marcello 
                TI  - Autocrine CXCL8-dependent invasiveness triggers modulation of actin cytoskeletal network and cell dynamics
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102733
                DO  - 10.18632/aging.102733
                SP  - 1928
                EP  - 1951
                PY  - 
                AB  - Glioblastoma (GB) is the most representative form of primary malignant brain tumour. Several studies indicated a pleiotropic role of CXCL8 in cancer due to its ability to modulate the tumour microenvironment, growth and aggressiveness of tumour cell. Previous studies indicated that CXCL8 by its receptors (CXCR1 and CXCR2) induced activation of the PI3K/p-Akt pathway, a crucial event in the regulation of cytoskeleton rearrangement and cell mobilization. Human GB primary cell culture and U-87MG cell line were used to study the effects of CXCR1 and CXCR2 blockage, by a dual allosteric antagonist, on cell migration and cytoskeletal dynamics. The data obtained point towards a specific effect of autocrine CXCL8 signalling on GB cell invasiveness by the activation of pathways involved in cell migration and cytoskeletal dynamics, such as PI3K/p-Akt/p-FAK, p-cortactin, RhoA, Cdc42, Acetylated &#x3B1;-tubulin and MMP2. All the data obtained support the concept that autocrine CXCL8 signalling plays a key role in the activation of an aggressive phenotype in primary glioblastoma cells and U-87MG cell line. These results provide new insights about the potential of a pharmacological approach targeting CXCR1/CXCR2 pathways to decrease migration and invasion of GB cells in the brain parenchyma, one of the principal mechanisms of recurrence.
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Association between serum levels of Klotho and inflammatory cytokines in cardiovascular disease: a case-control study

Ernesto Martín-Núñez, Javier Donate-Correa, Carla Ferri, Ángel López-Castillo, Alejandro Delgado-Molinos, Carolina Hernández-Carballo, Nayra Pérez-Delgado, Sergio Rodríguez-Ramos, Purificación Cerro-López, Víctor G. Tagua, Carmen Mora-Fernández, Juan F. Navarro-González,

https://doi.org/10.18632/aging.102734 pp 1952—1964

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Martín-Núñez E, Donate-Correa J, Ferri C, López-Castillo Á, Delgado-Molinos A, Hernández-Carballo C, Pérez-Delgado N, Rodríguez-Ramos S, Cerro-López P, Tagua VG, Mora-Fernández C, Navarro-González JF, . Association between serum levels of Klotho and inflammatory cytokines in cardiovascular disease: a case-control study. . 12:1952-1964. https://doi.org/10.18632/aging.102734

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                TY  - JOUR
                AU  - Martín-Núñez, Ernesto 
                AU  - Donate-Correa, Javier 
                AU  - Ferri, Carla 
                AU  - López-Castillo, Ángel 
                AU  - Delgado-Molinos, Alejandro 
                AU  - Hernández-Carballo, Carolina 
                AU  - Pérez-Delgado, Nayra 
                AU  - Rodríguez-Ramos, Sergio 
                AU  - Cerro-López, Purificación 
                AU  - Tagua, Víctor G. 
                AU  - Mora-Fernández, Carmen 
                AU  - Navarro-González, Juan F. 
                TI  - Association between serum levels of Klotho and inflammatory cytokines in cardiovascular disease: a case-control study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102734
                DO  - 10.18632/aging.102734
                SP  - 1952
                EP  - 1964
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Martín-Núñez, Ernesto 
                AU  - Donate-Correa, Javier 
                AU  - Ferri, Carla 
                AU  - López-Castillo, Ángel 
                AU  - Delgado-Molinos, Alejandro 
                AU  - Hernández-Carballo, Carolina 
                AU  - Pérez-Delgado, Nayra 
                AU  - Rodríguez-Ramos, Sergio 
                AU  - Cerro-López, Purificación 
                AU  - Tagua, Víctor G. 
                AU  - Mora-Fernández, Carmen 
                AU  - Navarro-González, Juan F. 
                TI  - Association between serum levels of Klotho and inflammatory cytokines in cardiovascular disease: a case-control study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102734
                DO  - 10.18632/aging.102734
                SP  - 1952
                EP  - 1964
                PY  - 
                AB  - Decrease in soluble anti-aging Klotho protein levels is associated to cardiovascular disease (CVD). Diverse studies have shown a bidirectional relationship between Klotho and inflammation, a risk factor for the development of CVD. In this work we aimed to evaluate the association between Klotho and inflammatory cytokines levels in the context of human CVD.The study included 110 patients with established CVD and preserved renal function, and a control group of 22 individuals without previous history of cardiovascular events. Serum Klotho and IL10 levels were significantly lower in the CVD group. Inflammatory status, marked by the TNF&#x3B1;/IL10 ratio and the C-reactive protein (CRP) levels, was significantly increased in the group of patients with established CVD. Soluble Klotho levels were directly correlated with eGFR (r=0.217) and IL10 (r=0.209) and inversely correlated with age (r=-0.261), CRP (r=-0.203), and TNF&#x3B1;/IL10 (r=-0.219). This association with TNF&#x3B1;/IL10 remained significant in age-matched subgroups. Multiple logistic regression analysis showed that age, smoking and the neutrophil-to-lymphocyte ratio (NLR) constituted risk factors for the presence of CVD, while Klotho was a protective factor.In conclusion, in patients with established CVD, the reduction in soluble Klotho is associated with a pro-inflammatory status marked by lower IL10 concentrations and higher TNF&#x3B1;/IL10 ratio and CRP levels.
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Anesthesia and surgery induce age-dependent changes in behaviors and microbiota

Ning Liufu, Ling Liu, Shiqian Shen, Zengliang Jiang, Yuanlin Dong, Yanyan Wang, Deborah Culley, Gregory Crosby, Minghui Cao, Yuan Shen, Edward Marcantonio, Zhongcong Xie, Yiying Zhang,

https://doi.org/10.18632/aging.102736 pp 1965—1986

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Liufu N, Liu L, Shen S, Jiang Z, Dong Y, Wang Y, Culley D, Crosby G, Cao M, Shen Y, Marcantonio E, Xie Z, Zhang Y, . Anesthesia and surgery induce age-dependent changes in behaviors and microbiota. . 12:1965-1986. https://doi.org/10.18632/aging.102736

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                TY  - JOUR
                AU  - Liufu, Ning 
                AU  - Liu, Ling 
                AU  - Shen, Shiqian 
                AU  - Jiang, Zengliang 
                AU  - Dong, Yuanlin 
                AU  - Wang, Yanyan 
                AU  - Culley, Deborah 
                AU  - Crosby, Gregory 
                AU  - Cao, Minghui 
                AU  - Shen, Yuan 
                AU  - Marcantonio, Edward 
                AU  - Xie, Zhongcong 
                AU  - Zhang, Yiying 
                TI  - Anesthesia and surgery induce age-dependent changes in behaviors and microbiota
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102736
                DO  - 10.18632/aging.102736
                SP  - 1965
                EP  - 1986
                PY  - 
                AB  - The neuropathogenesis of postoperative delirium remains mostly unknown. The gut microbiota is implicated in the pathogenesis of neurological disorders. We, therefore, set out to determine whether anesthesia/surgery causes age-dependent gut microbiota dysbiosis, changes in brain IL-6 level and mitochondrial function, leading to postoperative delirium-like behavior in mice. Female 9 or 18 months old mice received abdominal surgery under 1.4% isoflurane for two hours. The postoperative delirium-like behavior, gut microbiota, levels of brain IL-6, PSD-95 and synaptophysin, and mitochondrial function were determined by a battery of behavioral tests, 16s rRNA sequencing, ELISA, Western blot and Seahorse XFp Extracellular Flux Analyzer. Intragastric administration of Lactobacillus (10 days) and probiotic (20 days) were used to mitigate the anesthesia/surgery-induced changes. Anesthesia/surgery caused different alterations in gut microbiota, including change rate of reduction in the levels of gut lactobacillus, between the 18 and 9 months old mice. The anesthesia/surgery induced greater postoperative delirium-like behavior, increased brain IL-6 levels, decreased PSD-95 and synaptophysin levels, and mitochondrial dysfunction in 18 than 9 months old mice. Treatments with Lactobacillus and probiotic mitigated the anesthesia/surgery-induced changes. These data suggest that microbiota dysbiosis may contribute to neuropathogenesis of postoperative delirium and treatment with Lactobacillus or a probiotic could mitigate postoperative delirium.
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Paracrine senescence of human endometrial mesenchymal stem cells: a role for the insulin-like growth factor binding protein 3

Irina Vassilieva, Vera Kosheverova, Mikhail Vitte, Rimma Kamentseva, Alla Shatrova, Natalia Tsupkina, Elena Skvortsova, Aleksandra Borodkina, Elena Tolkunova, Nikolay Nikolsky, Elena Burova,

https://doi.org/10.18632/aging.102737 pp 1987—2004

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Vassilieva I, Kosheverova V, Vitte M, Kamentseva R, Shatrova A, Tsupkina N, Skvortsova E, Borodkina A, Tolkunova E, Nikolsky N, Burova E, . Paracrine senescence of human endometrial mesenchymal stem cells: a role for the insulin-like growth factor binding protein 3. . 12:1987-2004. https://doi.org/10.18632/aging.102737

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Provider: 
                TY  - JOUR
                AU  - Vassilieva, Irina 
                AU  - Kosheverova, Vera 
                AU  - Vitte, Mikhail 
                AU  - Kamentseva, Rimma 
                AU  - Shatrova, Alla 
                AU  - Tsupkina, Natalia 
                AU  - Skvortsova, Elena 
                AU  - Borodkina, Aleksandra 
                AU  - Tolkunova, Elena 
                AU  - Nikolsky, Nikolay 
                AU  - Burova, Elena 
                TI  - Paracrine senescence of human endometrial mesenchymal stem cells: a role for the insulin-like growth factor binding protein 3
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102737
                DO  - 10.18632/aging.102737
                SP  - 1987
                EP  - 2004
                PY  - 
                AB  - Stress-induced premature cell senescence is well recognized to be accompanied by emerging the senescence-associated secretory phenotype (SASP). Secreted SASP factors can promote the senescence of normal neighboring cells through autocrine/paracrine pathways and regulate the senescence response, as well. Regarding human endometrium-derived mesenchymal stem cells (MESCs), the SASP regulation mechanisms as well as paracrine activity of senescent cells have not been studied yet. Here, we examined the role of insulin-like growth factor binding protein 3 (IGFBP3) in the paracrine senescence induction in young MESCs. The H2O2-induced premature senescence of MESCs led to increased IGFBP3 in conditioned media (CM). The inhibitory analysis of both MAPK and PI3K signaling pathways showed that IGFBP3 releasing from senescent cells is mainly regulated by PI3K/Akt pathway activity. IGFBP3 appears to be an important senescence-mediating factor as its immunodepletion from the senescent CM weakened the pro-senescent effect of CM on young MESCs and promoted their growth. In contrast, young MESCs acquired the senescence phenotype in response to simultaneous addition of recombinant IGFBP3 (rIGFBP3). The mechanism of extracellular IGFBP3 internalization was also revealed. The present study is the first to demonstrate a significant role of extracellular IGFBP3 in paracrine senescence induction of young MESCs.
                ER  -

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Late-life obesity is a protective factor for prodromal Alzheimer’s disease: a longitudinal study

Zhen Sun, Zuo-Teng Wang, Fu-Rong Sun, Xue-Ning Shen, Wei Xu, Ya-Hui Ma, Qiang Dong, Lan Tan, Jin-Tai Yu, Alzheimer’s Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.102738 pp 2005—2017

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Sun Z, Wang Z, Sun F, Shen X, Xu W, Ma Y, Dong Q, Tan L, Yu J, , . Late-life obesity is a protective factor for prodromal Alzheimer’s disease: a longitudinal study. . 12:2005-2017. https://doi.org/10.18632/aging.102738

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                TY  - JOUR
                AU  - Sun, Zhen 
                AU  - Wang, Zuo-Teng 
                AU  - Sun, Fu-Rong 
                AU  - Shen, Xue-Ning 
                AU  - Xu, Wei 
                AU  - Ma, Ya-Hui 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                AU  - ,  
                TI  - Late-life obesity is a protective factor for prodromal Alzheimer’s disease: a longitudinal study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102738
                DO  - 10.18632/aging.102738
                SP  - 2005
                EP  - 2017
                PY  - 
                AB  - Higher body mass index (BMI) in late-life has recently been considered as a possible protective factor for Alzheimer&apos;s disease (AD), which yet remains conflicting. To test this hypothesis, we have evaluated the cross-sectional and longitudinal associations of BMI categories with CSF biomarkers, brain &#x3B2;-amyloid (A&#x3B2;) load, brain structure, and cognition and have assessed the effect of late-life BMI on AD risk in a large sample (n = 1,212) of non-demented elderly from the Alzheimer&#x2019;s Disease Neuroimaging Initiative (ADNI) database. At baseline, higher late-life BMI categories were associated with higher levels of CSF A&#x3B2;42 (p=0.037), lower levels of CSF total-tau (t-tau, p=0.026) and CSF t-tau/A&#x3B2;42 (p=0.008), lower load of A&#x3B2; in the right hippocampus (p=0.030), as well as larger volumes of hippocampus (p&lt;0.0001), entorhinal cortex (p=0.009) and middle temporal lobe (p=0.040). But no association was found with CSF phosphorylated-tau (p-tau) or CSF p-tau/A&#x3B2;42. Longitudinal studies showed that higher BMI individuals experienced a slower decline in cognitive function. In addition, Kaplan&#x2013;Meier survival analysis revealed that higher late-life BMI had a reduced risk of progression to AD over time (p = 0.009). Higher BMI in late-life decreased the risk of AD, and this process may be driven by AD-related biomarkers.
                ER  -

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Correction for: Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes

Qi Peng, Bin Chen, Hao Wang, Ying Zhu, Jinghong Wu, Yetao Luo, Guowei Zu, Jinyong Luo, Lan Zhou, Qiong Shi, Yaguang Weng, Ailong Huang, Tong-Chuan He, Jiaming Fan,

https://doi.org/10.18632/aging.102759 pp 2018—2021

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Peng Q, Chen B, Wang H, Zhu Y, Wu J, Luo Y, Zu G, Luo J, Zhou L, Shi Q, Weng Y, Huang A, He T, et al, . Correction for: Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes. . 12:2018-2021. https://doi.org/10.18632/aging.102759

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                TY  - JOUR
                AU  - Peng, Qi 
                AU  - Chen, Bin 
                AU  - Wang, Hao 
                AU  - Zhu, Ying 
                AU  - Wu, Jinghong 
                AU  - Luo, Yetao 
                AU  - Zu, Guowei 
                AU  - Luo, Jinyong 
                AU  - Zhou, Lan 
                AU  - Shi, Qiong 
                AU  - Weng, Yaguang 
                AU  - Huang, Ailong 
                AU  - He, Tong-Chuan 
                AU  - Fan, Jiaming 
                TI  - Correction for: Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102759
                DO  - 10.18632/aging.102759
                SP  - 2018
                EP  - 2021
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Peng, Qi 
                AU  - Chen, Bin 
                AU  - Wang, Hao 
                AU  - Zhu, Ying 
                AU  - Wu, Jinghong 
                AU  - Luo, Yetao 
                AU  - Zu, Guowei 
                AU  - Luo, Jinyong 
                AU  - Zhou, Lan 
                AU  - Shi, Qiong 
                AU  - Weng, Yaguang 
                AU  - Huang, Ailong 
                AU  - He, Tong-Chuan 
                AU  - Fan, Jiaming 
                TI  - Correction for: Bone morphogenetic protein 4 (BMP4) alleviates hepatic steatosis by increasing hepatic lipid turnover and inhibiting the mTORC1 signaling axis in hepatocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102759
                DO  - 10.18632/aging.102759
                SP  - 2018
                EP  - 2021
                PY  - 
                AB  - 
                ER  -

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Volume 12, Issue 2

About the Cover

Editorials

Ana Paula Tagliari, Maurizio Taramasso,

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Victorine Douin-Echinard, Lise Lefevre, Angelo Parini,

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Mukul Girotra, Olaia Naveiras, Nicola Vannini,

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Stefanie Müthel, Baris Tursun,

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Research Papers

Weiyu Xu, Si Yu, Jianping Xiong, Junyu Long, Yongchang Zheng, Xinting Sang,

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Xiaofeng Feng, Jianying Pan, Junyan Li, Chun Zeng, Weizhong Qi, Yan Shao, Xin Liu, Liangliang Liu, Guozhi Xiao, Haiyan Zhang, Xiaochun Bai, Daozhang Cai,

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Kuan-Yu Lai, Tai-Hsien Wu, Chiu-Shong Liu, Chih-Hsueh Lin, Cheng-Chieh Lin, Ming-May Lai, Wen-Yuan Lin,

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Guan Sun, Ying Cao, Chunfa Qian, Zhengqiang Wan, Jian Zhu, Jun Guo, Lei Shi,

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Yan Zhang, Xiu-Juan Xu, Ting-Yu Lian, Ling-Feng Huang, Jin-Mei Zeng, Dong-Mei Liang, Ming-Juan Yin, Jing-Xiao Huang, Liang-Chang Xiu, Zu-Wei Yu, Yu-Lian Li, Chen Mao, Jin-Dong Ni,

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Jian Wang, Mengchan Zhu, Ling Ye, Cuicui Chen, Jun She, Yuanlin Song,

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Jinqian Liang, Ying-chao Shen, Xiang-yang Zhang, Chong Chen, Hong Zhao, Jianhua Hu,

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Shuncong Wang, Haiqing Ma, Xuemin Li, Xiangqiong Mo, Haiyu Zhang, Lewei Yang, Yun Deng, Yan Yan, Guangwei Yang, Xingwei Liu, Huanhuan Sun,

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Lingjing Liu, Chenjian Song, Jingli Li, Qiang Wang, Mingyang Zhu, Yiran Hu, Junjie Chen, Chaolei Chen, Jin-San Zhang, Nian Dong, Chengshui Chen,

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Shumpei Fujie, Natsuki Hasegawa, Kiyoshi Sanada, Takafumi Hamaoka, Seiji Maeda, Jaume Padilla, Luis A. Martinez-Lemus, Motoyuki Iemitsu,

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Zhuochao Liu, Junxiang Wen, Chuanlong Wu, Chuanzhen Hu, Jun Wang, Qiyuan Bao, Hongyi Wang, Jizhuang Wang, Qi Zhou, Li Wei, Yuhui Shen, Weibin Zhang,

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Xingming Jiang, Jinglin Li, Weina Wang, Zengtao Hu, Canghai Guan, Yuqiao Zhao, Wenzhi Li, Yunfu Cui,

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Ying-Jie Niu, Wenjun Zhou, Zheng-Wen Nie, Dongjie Zhou, Yong-Nan Xu, Sun A. Ock, Chang-Guo Yan, Xiang-Shun Cui,

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Chi Zhang, Yun Xie, Haicheng Chen, Linyan Lv, Jiahui Yao, Min Zhang, Kai Xia, Xin Feng, Yanqing Li, Xiaoyan Liang, Xiangzhou Sun, Chunhua Deng, Guihua Liu,

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Man Li, Anqi Lin, Peng Luo, Weitao Shen, Dan Xiao, Lanying Gou, Jian Zhang, Linlang Guo,

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