Volume 11, Issue 18

Chen P, Chen F, Zhou B, . Leonurine ameliorates D-galactose-induced aging in mice through activation of the Nrf2 signalling pathway. . 11:7339-7356. https://doi.org/10.18632/aging.101733

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                TY  - JOUR
                AU  - Chen, Peng 
                AU  - Chen, Fuchao 
                AU  - Zhou, Ben-hong 
                TI  - Leonurine ameliorates D-galactose-induced aging in mice through activation of the Nrf2 signalling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101733
                DO  - 10.18632/aging.101733
                SP  - 7339
                EP  - 7356
                PY  - 
                AB  - Aging is a complex physiological phenomenon associated with oxidative stress damage. The objective of this study was to investigate the potential effects of leonurine on D-galactose-induced aging in mice and its possible mechanisms. In this study, we first tested the antioxidant activity of leonurine in vitro. A subcutaneous injection of D-galactose in mice for 8 weeks was used to establish the aging model to evaluate the protective effects of leonurine. The results showed that treatment with 150 mg&#xB7;kg-1 leonurine could improve the mental condition, organic index, and behavioural impairment; significantly increase the activities of antioxidative enzymes including SOD, CAT, and T-AOC; and ameliorate the advanced glycation end product (AGE) level and histopathological injury. Furthermore, the Western blotting data revealed that leonurine supplementation noticeably modulated the suppression of the Nrf2 pathway and upregulated the downstream expression of HO-1 and NOQ1 in aging mice. Additionally, leonurine treatment activated Nrf2 nuclear translocation in both aging mice and normal young mice, and the expression levels of Nrf2 in normal young mice was higher than those in naturally aging mice. In conclusion, our findings suggest that leonurine is a promising agent for attenuating the aging process, and the underlying molecular mechanisms depend on activating the Nrf2 pathway.
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miR-375-3p suppresses tumorigenesis and partially reverses chemoresistance by targeting YAP1 and SP1 in colorectal cancer cells

Xueni Xu, Xiaoxiang Chen, Mu Xu, Xiangxiang Liu, Bei Pan, Jian Qin, Tao Xu, Kaixuan Zeng, Yuqin Pan, Bangshun He, Huiling Sun, Li Sun, Shukui Wang,

https://doi.org/10.18632/aging.102214 pp 7357—7385

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Xu X, Chen X, Xu M, Liu X, Pan B, Qin J, Xu T, Zeng K, Pan Y, He B, Sun H, Sun L, Wang S, . miR-375-3p suppresses tumorigenesis and partially reverses chemoresistance by targeting YAP1 and SP1 in colorectal cancer cells. . 11:7357-7385. https://doi.org/10.18632/aging.102214

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                TY  - JOUR
                AU  - Xu, Xueni 
                AU  - Chen, Xiaoxiang 
                AU  - Xu, Mu 
                AU  - Liu, Xiangxiang 
                AU  - Pan, Bei 
                AU  - Qin, Jian 
                AU  - Xu, Tao 
                AU  - Zeng, Kaixuan 
                AU  - Pan, Yuqin 
                AU  - He, Bangshun 
                AU  - Sun, Huiling 
                AU  - Sun, Li 
                AU  - Wang, Shukui 
                TI  - miR-375-3p suppresses tumorigenesis and partially reverses chemoresistance by targeting YAP1 and SP1 in colorectal cancer cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102214
                DO  - 10.18632/aging.102214
                SP  - 7357
                EP  - 7385
                PY  - 
                AB  - Clinically, one of the principal factors in the failure of advanced colorectal cancer (CRC) treatment is chemoresistance to 5-fluorouracil (5FU)-based chemotherapy. Although microRNA-375-3p (miR-375) is considered a tumor suppressor in multiple cancers, the mechanism of miR-375 in the regulation of drug resistance in CRC remains unclear. In this study, we investigated the chemosensitivity of miR-375 to 5FU in CRC from biological and clinical aspects. We found that miR-375 was significantly downregulated in CRC tissues and cell lines, and low miR-375 expression was strongly correlated with poor overall survival in CRC patients. Overexpression of miR-375 sensitized CRC cells to a broad spectrum of chemotherapeutic drugs in vitro and in vivo. Further mechanistic analysis demonstrated that miR-375 enhanced CRC cell sensitivity to 5FU by directly targeting YAP1 and SP1. MiR-375 downregulated YAP1, resulting in reduced expression of the Hippo-YAP1 pathway downstream genes CTGF, cyclin D1 and BIRC5 (also known as survivin). Overall, miR-375 was confirmed as a prospective molecular biomarker in the chemoresistance and prognosis of CRC patients, and the synergy between miR-375 and chemotherapeutic drugs could be a promising therapeutic strategy for CRC patients, especially with chemoresistance.
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lncRNA DLEU2 modulates cell proliferation and invasion of non-small cell lung cancer by regulating miR-30c-5p/SOX9 axis

Yongchun Zhou, Hutao Shi, Yaqian Du, Guangqiang Zhao, Xiaoxiong Wang, Quan Li, Junxi Liu, Lianhua Ye, Zhenghai Shen, Yinjin Guo, Yunchao Huang,

https://doi.org/10.18632/aging.102226 pp 7386—7401

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Zhou Y, Shi H, Du Y, Zhao G, Wang X, Li Q, Liu J, Ye L, Shen Z, Guo Y, Huang Y, . lncRNA DLEU2 modulates cell proliferation and invasion of non-small cell lung cancer by regulating miR-30c-5p/SOX9 axis. . 11:7386-7401. https://doi.org/10.18632/aging.102226

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                TY  - JOUR
                AU  - Zhou, Yongchun 
                AU  - Shi, Hutao 
                AU  - Du, Yaqian 
                AU  - Zhao, Guangqiang 
                AU  - Wang, Xiaoxiong 
                AU  - Li, Quan 
                AU  - Liu, Junxi 
                AU  - Ye, Lianhua 
                AU  - Shen, Zhenghai 
                AU  - Guo, Yinjin 
                AU  - Huang, Yunchao 
                TI  - lncRNA DLEU2 modulates cell proliferation and invasion of non-small cell lung cancer by regulating miR-30c-5p/SOX9 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102226
                DO  - 10.18632/aging.102226
                SP  - 7386
                EP  - 7401
                PY  - 
                AB  - Increasing evidence indicated that long noncoding RNAs (lncRNA) play critical roles in the progression of multiple cancers and that dysregulation of lncRNA promotes tumor progression. However, the function and underlying mechanism of lncRNA DLEU2 in biological behaviors of NSCLC cells are still largely unknown. Our studies confirmed that lncRNA DLEU2 was highly expressed in NSCLC tissues and cell lines, which was correlated with shorter overall survival in NSCLC patients. In vitro, knockdown of lncRNA DLEU2 inhibited proliferation, invasion, migration and induced apoptosis of both A549 and LLC cells; In vivo, it suppressed tumor growth and metastasis. lncRNA DLEU2 directly interacted with miR-30c-5p, which further targeted SOX9 and exerted oncogenic functions in NSCLC. Mechanistically, overexpression of lncRNA DLEU2 exhibits tumorigenic effects through downregulating the inhibitory effect of miR-30c-5p on SOX9 expression. In conclusion, Our finding confirmed that lncRNA DLEU2 as a novel oncogenic in NSCLC, which provide a potential novel diagnostic and therapeutic target for NSCLC.
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CCL28 promotes locomotor recovery after spinal cord injury via recruiting regulatory T cells

Pengfei Wang, Xiangbei Qi, Guohui Xu, Jianning Liu, Jichao Guo, Xu Li, Xinzhe Ma, Hui Sun,

https://doi.org/10.18632/aging.102239 pp 7402—7415

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Wang P, Qi X, Xu G, Liu J, Guo J, Li X, Ma X, Sun H, . CCL28 promotes locomotor recovery after spinal cord injury via recruiting regulatory T cells. . 11:7402-7415. https://doi.org/10.18632/aging.102239

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                TY  - JOUR
                AU  - Wang, Pengfei 
                AU  - Qi, Xiangbei 
                AU  - Xu, Guohui 
                AU  - Liu, Jianning 
                AU  - Guo, Jichao 
                AU  - Li, Xu 
                AU  - Ma, Xinzhe 
                AU  - Sun, Hui 
                TI  - CCL28 promotes locomotor recovery after spinal cord injury via recruiting regulatory T cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102239
                DO  - 10.18632/aging.102239
                SP  - 7402
                EP  - 7415
                PY  - 
                AB  - Background: Chemokines play a key role in post-traumatic inflammation and secondary injury after spinal cord injury (SCI). CCL28, the chemokine CC-chemokine ligand 28, is involved in the epithelial and mucosal immunity. However, whether CCL28 participates in the physiopathologic processes after SCI remains unclear.Results: CCL28 is upregulated in the spinal cord after SCI. In addition, neutralizing antibodies against IL-1&#x3B2; or TNF-&#x3B1;, or treatment of ML120B, a selective inhibitor of IKK-&#x3B2;, remarkably decrease CCL28 upregulation, suggesting that CCL28 upregulation relies on NF-&#x3BA;B pathway activated by IL-1&#x3B2; and TNF-&#x3B1; after SCI. Moreover, CD4+CD25+FOXP3+ regulatory T (Treg) cells that express CCR10, a receptor of CCL28, are enriched in the spinal cord after SCI. We further demonstrate that the spinal cord recruits Treg cells through CCL28-CCR10 axis, which in turn function to suppress immune response and promote locomotor recovery after SCI. In contrast, neutralizing CCL28 or CCR10 reduces Treg cell recruitment and delays locomotor recovery.Methods: The neutralizing antibodies and recombinant CCL28 were injected intraspinally into the mice prior to SCI, which was established via hemitransection. RT-qPCR analysis was performed to determine transcript level, and Western blot analysis and ELISA assay were used to detect protein expression. Immune cells were analyzed by flow cytometry and visualized by immunofluorescence. The chemotaxis was assessed by in vitro transwell migration assay. The mouse locomotor activity was assessed via the Basso Mouse Scale (BMS) system.Conclusions: These results indicate that NF-&#x3BA;B pathway-regulated CCL28 production plays a protective role after SCI through recruiting CCR10-expressing and immunosuppressive Treg cells, and suggest that interfering CCL28-CCR10 axis might be of potential clinical benefit in improving SCI recovery.
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Hearing consequences in Gjb2 knock-in mice: implications for human p.V37I mutation

Xin Lin, Gen Li, Yu Zhang, Jingjing Zhao, Jiawen Lu, Yunge Gao, Huihui Liu, Geng-Lin Li, Tao Yang, Lei Song, Hao Wu,

https://doi.org/10.18632/aging.102246 pp 7416—7441

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Lin X, Li G, Zhang Y, Zhao J, Lu J, Gao Y, Liu H, Li G, Yang T, Song L, Wu H, . Hearing consequences in Gjb2 knock-in mice: implications for human p.V37I mutation. . 11:7416-7441. https://doi.org/10.18632/aging.102246

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                TY  - JOUR
                AU  - Lin, Xin 
                AU  - Li, Gen 
                AU  - Zhang, Yu 
                AU  - Zhao, Jingjing 
                AU  - Lu, Jiawen 
                AU  - Gao, Yunge 
                AU  - Liu, Huihui 
                AU  - Li, Geng-Lin 
                AU  - Yang, Tao 
                AU  - Song, Lei 
                AU  - Wu, Hao 
                TI  - Hearing consequences in Gjb2 knock-in mice: implications for human p.V37I mutation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102246
                DO  - 10.18632/aging.102246
                SP  - 7416
                EP  - 7441
                PY  - 
                AB  - Human p.V37I mutation of GJB2 gene was strongly correlated with late-onset progressive hearing loss, especially among East Asia populations. We generated a knock-in mouse model based on human p.V37I variant (c.109G&gt;A) that recapitulated the human phenotype. Cochlear pathology revealed no significant hair cell loss, stria vascularis atrophy or spiral ganglion neuron loss, but a significant change in the length of gap junction plaques, which may have contributed to the observed mild endocochlear potential (EP) drop in homozygous mice lasting lifetime. The cochlear amplification in homozygous mice was compromised, but outer hair cells&#x2019; function remained unchanged, indicating that the reduced amplification was EP- rather than prestin-generated. In addition to ABR threshold elevation, ABR wave I latencies were also prolonged in aged homozygous animals. We found in homozygous IHCs a significant increase in ICa but no change in Ca2+ efficiency in triggering exocytosis. Environmental insults such as noise exposure, middle ear injection of KCl solution and systemic application of furosemide all exacerbated the pathological phenotype in homozygous mice. We conclude that this Gjb2 mutation-induced hearing loss results from 1) reduced cochlear amplifier caused by lowered EP, 2) IHCs excitotoxicity associated with potassium accumulation around hair cells, and 3) progression induced by environmental insults.
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Analyses of an epigenetic switch involved in the activation of pioneer factor FOXA1 leading to the prognostic value of estrogen receptor and FOXA1 co-expression in breast cancer

Xuan Jing, Hongping Liang, Chonghua Hao, Li Hongxia, Xiangrong Cui,

https://doi.org/10.18632/aging.102250 pp 7442—7456

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Jing X, Liang H, Hao C, Hongxia L, Cui X, . Analyses of an epigenetic switch involved in the activation of pioneer factor FOXA1 leading to the prognostic value of estrogen receptor and FOXA1 co-expression in breast cancer. . 11:7442-7456. https://doi.org/10.18632/aging.102250

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                TY  - JOUR
                AU  - Jing, Xuan 
                AU  - Liang, Hongping 
                AU  - Hao, Chonghua 
                AU  - Hongxia, Li 
                AU  - Cui, Xiangrong 
                TI  - Analyses of an epigenetic switch involved in the activation of pioneer factor FOXA1 leading to the prognostic value of estrogen receptor and FOXA1 co-expression in breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102250
                DO  - 10.18632/aging.102250
                SP  - 7442
                EP  - 7456
                PY  - 
                AB  - Forkhead box protein A1 (FOXA1) is a pioneer factor of estrogen receptor &#x3B1; (ER)&#x2013;chromatin binding and function, yet the role of FOXA1 in breast cancer and the underlying molecular mechanisms have not yet been elucidated. To evaluate gene expression alterations during breast carcinogenesis, FOXA1 expression was analyzed using the Serial Analysis of Gene Expression Genie suite, a gene expression profiling interactive analysis, and Oncomine analyses. The correlation between methylation and expression was analyzed using the MEXPRESS tool and UCSC Xena browser. Then, the expression and prognostic value of FOXA1 was validated by our own breast cancer samples using RT-PCR. We obtained the following important results. (1) The expression level of FOXA1 was significantly higher in breast cancer than normal tissues. (2) ER, PR, HEGR-2, and nodal status were positively correlated with FOXA1 expression. (3) Among patients with ER+ tumors, those with higher FOXA1 expression levels had better survival probabilities. (4) The major mutation type in FOXA1 in breast cancer samples was missense mutations. (5) FOXA1 expression was significantly higher in ER+ breast tumors than in ER&#x2212; tumors or normal tissues. Our findings suggest that the aberrant DNA hypomethylation of promoter regions is one mechanism underlying the aberrant expression of FOXA1 in ER+ breast cancer, which might be a potential indicator of favorable prognosis.
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Increased interleukin-18 level contributes to the development and severity of ischemic stroke

Yong Hao, Jie Ding, Ronghua Hong, Shuwei Bai, Ze Wang, Chengjun Mo, Qiang Hu, Zezhi Li, Yangtai Guan,

https://doi.org/10.18632/aging.102253 pp 7457—7472

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Hao Y, Ding J, Hong R, Bai S, Wang Z, Mo C, Hu Q, Li Z, Guan Y, . Increased interleukin-18 level contributes to the development and severity of ischemic stroke. . 11:7457-7472. https://doi.org/10.18632/aging.102253

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                TY  - JOUR
                AU  - Hao, Yong 
                AU  - Ding, Jie 
                AU  - Hong, Ronghua 
                AU  - Bai, Shuwei 
                AU  - Wang, Ze 
                AU  - Mo, Chengjun 
                AU  - Hu, Qiang 
                AU  - Li, Zezhi 
                AU  - Guan, Yangtai 
                TI  - Increased interleukin-18 level contributes to the development and severity of ischemic stroke
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102253
                DO  - 10.18632/aging.102253
                SP  - 7457
                EP  - 7472
                PY  - 
                AB  - Although interleukin-18 (IL-18) has been implicated in the pathophysiology of stroke, research findings concerning IL-18 level in stroke have been inconsistent. Thus, we performed a cross-sectional study in patients with first-episode ischemic stroke and then extracted relevant data from databases to validate our results. A total of 252 patients and 259 healthy subjects were recruited, and serum IL-18 level was evaluated in a cross-sectional study. Then, we extracted data and conducted a meta-analysis, including 2,928 patients and 3,739 controls to support our results. A 95% confidence interval for standardized mean difference (SMD) was calculated using a Z test. We found IL-18 was higher in stroke patients than in controls (2.39 &#xB1; 0.25 vs. 2.25 &#xB1; 0.28, F=8.60, p=0.004) and was negatively associated with the NIHSS scale (r = -0.14, p=0.028). A subsequent meta-analysis confirmed that IL-18 level was higher in stroke patients than in controls (SMD = 2.14, 95% CI = 1.54 &#x223C; 2.73, P&lt; 0.001). IL-18 level increased with the severity of the stroke (p&lt; 0.01). These findings revealed increased IL-18 level contributed to the development and severity of ischemic stroke, suggesting the potential of this biomarker to become an important reference for the early monitoring of ischemic stroke.
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HnRNPR-CCNB1/CENPF axis contributes to gastric cancer proliferation and metastasis

Er-Bao Chen, Xuan Qin, Ke Peng, Qian Li, Cheng Tang, Yi-Chou Wei, Shan Yu, Lu Gan, Tian-Shu Liu,

https://doi.org/10.18632/aging.102254 pp 7473—7491

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Chen E, Qin X, Peng K, Li Q, Tang C, Wei Y, Yu S, Gan L, Liu T, . HnRNPR-CCNB1/CENPF axis contributes to gastric cancer proliferation and metastasis. . 11:7473-7491. https://doi.org/10.18632/aging.102254

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                TY  - JOUR
                AU  - Chen, Er-Bao 
                AU  - Qin, Xuan 
                AU  - Peng, Ke 
                AU  - Li, Qian 
                AU  - Tang, Cheng 
                AU  - Wei, Yi-Chou 
                AU  - Yu, Shan 
                AU  - Gan, Lu 
                AU  - Liu, Tian-Shu 
                TI  - HnRNPR-CCNB1/CENPF axis contributes to gastric cancer proliferation and metastasis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102254
                DO  - 10.18632/aging.102254
                SP  - 7473
                EP  - 7491
                PY  - 
                AB  - Gastric cancer (GC) is a common disease globally with high mortality rate. It is therefore necessary to develop novel therapies targeting specific events in the pathogenesis of GC. Some hnRNP family members are involved in multiple cancer biological behaviors. However, the potential function and mechanism of hnRNPR, a new molecule of hnRNP family in GC remains unknown. We found that the expression of hnRNPR was significantly overexpressed in multiple cancers compared to the normal tissues. Functionally, hnRNPR promoted cancer cell proliferation, migration, and invasion. Knockdown of hnRNPR in two type mice models, with two types of tumors models decreased the tumor aggressiveness and metastasis. Mechanistically, hnRNPR targeted oncogenic pathways by stabilizing the expression of CCNB1 and CENPF mRNA level. Knockdown of CCNB1 and CENPF abolished the hnRNPR-induced cell growth and invasion, respectively. Furthermore, the protein level of hnRNPR in the tumor was positively correlated with the expression of CCNB1 and CENPF in clinical samples. Together, these results indicate that overexpression of hnRNPR promoted the aggressiveness of GC by increasing the mRNA expression of CCNB1 and CENPF. HnRNPR-CCNB1/CENPF axis may be a potential therapeutic target for GC treatment.
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PTEN loss regulates alveolar epithelial cell senescence in pulmonary fibrosis depending on Akt activation

Ting Qiu, Yaqiong Tian, Yujuan Gao, Miao Ma, Hui Li, Xiaoqin Liu, Hongyan Wu, Yingwei Zhang, Hui Ding, Mengshu Cao, Ji Zhang, Jinghong Dai, Jingyu Chen, Hourong Cai,

https://doi.org/10.18632/aging.102262 pp 7492—7509

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Qiu T, Tian Y, Gao Y, Ma M, Li H, Liu X, Wu H, Zhang Y, Ding H, Cao M, Zhang J, Dai J, Chen J, et al, . PTEN loss regulates alveolar epithelial cell senescence in pulmonary fibrosis depending on Akt activation. . 11:7492-7509. https://doi.org/10.18632/aging.102262

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                TY  - JOUR
                AU  - Qiu, Ting 
                AU  - Tian, Yaqiong 
                AU  - Gao, Yujuan 
                AU  - Ma, Miao 
                AU  - Li, Hui 
                AU  - Liu, Xiaoqin 
                AU  - Wu, Hongyan 
                AU  - Zhang, Yingwei 
                AU  - Ding, Hui 
                AU  - Cao, Mengshu 
                AU  - Zhang, Ji 
                AU  - Dai, Jinghong 
                AU  - Chen, Jingyu 
                AU  - Cai, Hourong 
                TI  - PTEN loss regulates alveolar epithelial cell senescence in pulmonary fibrosis depending on Akt activation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102262
                DO  - 10.18632/aging.102262
                SP  - 7492
                EP  - 7509
                PY  - 
                AB  - Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease with poor prognosis. The mechanisms underlying the role of alveolar epithelial cell (AEC) senescence in IPF remain poorly understood. We aimed to investigate if PTEN/Akt activates AEC senescence to induce pulmonary fibrosis. We investigated the association between PTEN/Akt and cellular senescence in lung tissues from IPF patients. As a result, decreased PTEN and activated Akt pathway were found in AECs in fibrotic lung tissues detected by immunohistochemistry (IHC) and immunofluorescence (IF). Increased expression levels of aging-associated markers (P21WAF1 and SA-&#x3B2;-gal) in AECs treated with bleomycin were found. AEC senescence was accelerated by PTEN knockdown and attenuated by PTEN overexpression. Bleomycin induced AEC senescence was reversed by Akt2 knockdown and the pharmacological inhibitors (LY294002 and MK2206) of the Akt pathway. Reducing Akt activation dramatically improved lung fibrosis in a fibrotic mice model. In addition, a co-immunoprecipitation (co-IP) assay demonstrated that PTEN physically associated with Akt. These indicated that senescent AECs modulated by the PTEN/Akt pathway promote lung fibrosis. In conclusion, our study demonstrated that as a trigger indicator in IPF, the senescence process in AECs should be a potential therapeutic target and that the PTEN/Akt pathway may be a promising candidate for intervention.
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MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling

Tianbao Chen, Yi Zhang, Yilan Liu, Dexiao Zhu, Jing Yu, Guoqian Li, Zhichun Sun, Wanru Wang, Hongwei Jiang, Zhenzhen Hong,

https://doi.org/10.18632/aging.102263 pp 7510—7524

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Chen T, Zhang Y, Liu Y, Zhu D, Yu J, Li G, Sun Z, Wang W, Jiang H, Hong Z, . MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling. . 11:7510-7524. https://doi.org/10.18632/aging.102263

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                TY  - JOUR
                AU  - Chen, Tianbao 
                AU  - Zhang, Yi 
                AU  - Liu, Yilan 
                AU  - Zhu, Dexiao 
                AU  - Yu, Jing 
                AU  - Li, Guoqian 
                AU  - Sun, Zhichun 
                AU  - Wang, Wanru 
                AU  - Jiang, Hongwei 
                AU  - Hong, Zhenzhen 
                TI  - MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102263
                DO  - 10.18632/aging.102263
                SP  - 7510
                EP  - 7524
                PY  - 
                AB  - This study aimed to establish a high-fat diet (HFD)-fed obese mouse model and a cell culture model of insulin resistance (IR) in mature 3T3-L1 adipocytes. A dual-luciferase reporter assay (DLRA) was confirmed interaction between miR-27a and the 3&#x2032;-untranslated region (UTR) of Peroxisome proliferator-activated receptor (PPAR)-&#x3B3;. The inhibition of PPAR-&#x3B3; expression by microRNA (miR)-27a in IR cells at both the protein and mRNA levels was confirmed by a mechanistic investigation. Moreover, the 3&#x2032;-UTR of PPAR-&#x3B3; was found to be a direct target of miR-27a, based on the DLRA. Furthermore, antagomiR-27a upregulated the activation of PI3K/Akt signaling and glucose transporter type 4 (GLUT4) expression at the protein and mRNA levels. Additionally, the PPAR inhibitor T0070907 repressed the insulin sensitivity upregulated by antagomiR-27a, which was accompanied by the inhibition of PPAR-&#x3B3; expression and increased levels of AKT phosphorylation and GLUT4. The PI3K inhibitor wortmannin reduced miR-27a-induced increases in AKT phosphorylation, glucose uptake, and GLUT4. miR-27a is considered to be involved in the PPAR-&#x3B3;-PI3K/AKT-GLUT4 signaling axis, thus leading to increased glucose uptake and decreased IR in HFD-fed mice and 3T3-L1 adipocytes. Therefore, miR-27a is a novel target for the treatment of IR in obesity and diabetes.
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Identification of a novel microRNA recurrence-related signature and risk stratification system in breast cancer

Jianguo Lai, Bo Chen, Guochun Zhang, Yulei Wang, Hsiaopei Mok, Lingzhu Wen, Zihao Pan, Fengxi Su, Ning Liao,

https://doi.org/10.18632/aging.102268 pp 7525—7536

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Lai J, Chen B, Zhang G, Wang Y, Mok H, Wen L, Pan Z, Su F, Liao N, . Identification of a novel microRNA recurrence-related signature and risk stratification system in breast cancer. . 11:7525-7536. https://doi.org/10.18632/aging.102268

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                TY  - JOUR
                AU  - Lai, Jianguo 
                AU  - Chen, Bo 
                AU  - Zhang, Guochun 
                AU  - Wang, Yulei 
                AU  - Mok, Hsiaopei 
                AU  - Wen, Lingzhu 
                AU  - Pan, Zihao 
                AU  - Su, Fengxi 
                AU  - Liao, Ning 
                TI  - Identification of a novel microRNA recurrence-related signature and risk stratification system in breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102268
                DO  - 10.18632/aging.102268
                SP  - 7525
                EP  - 7536
                PY  - 
                AB  - Increasing evidence has revealed that microRNAs (miRNAs) play vital roles in breast cancer (BC) prognosis. Thus, we aimed to identify recurrence-related miRNAs and establish accurate risk stratification system in BC patients. A total of 381 differentially expressed miRNAs were confirmed by analyzing 1044 BC tissues and 102 adjacent normal samples from The Cancer Genome Atlas (TCGA). Then, based on the association between each miRNAs and disease-free survival (DFS), we identified miRNA recurrence-related signature to construct a novel prognostic nomogram using Cox regression model. Target genes of the four miRNAs were analyzed via Gene Ontology and KEGG pathway analyses. Time-dependent receiver operating characteristic analysis indicated that a combination of the miRNA signature and tumor-node-metastasis (TNM) stage had better predictive performance than that of TNM stage (0.710 vs 0.616, P&lt;0.0001). Furthermore, risk stratification analysis suggested that the miRNA-based model could significantly classify patients into the high- and low-risk groups in the two cohorts (all P&lt;0.0001), and was independent of other clinical features. Functional enrichment analysis demonstrated that the 46 target genes mainly enrichment in important cell biological processes, protein binding and cancer-related pathways. The miRNA-based prognostic model may facilitate individualized treatment decisions for BC patients.
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Hydrogen sulfide is a novel regulator implicated in glucocorticoids-inhibited bone formation

Jun Ma, Changgui Shi, Zhongyang Liu, Bin Han, Lei Guo, Lei Zhu, Tianwen Ye,

https://doi.org/10.18632/aging.102269 pp 7537—7552

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Ma J, Shi C, Liu Z, Han B, Guo L, Zhu L, Ye T, . Hydrogen sulfide is a novel regulator implicated in glucocorticoids-inhibited bone formation. . 11:7537-7552. https://doi.org/10.18632/aging.102269

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                TY  - JOUR
                AU  - Ma, Jun 
                AU  - Shi, Changgui 
                AU  - Liu, Zhongyang 
                AU  - Han, Bin 
                AU  - Guo, Lei 
                AU  - Zhu, Lei 
                AU  - Ye, Tianwen 
                TI  - Hydrogen sulfide is a novel regulator implicated in glucocorticoids-inhibited bone formation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102269
                DO  - 10.18632/aging.102269
                SP  - 7537
                EP  - 7552
                PY  - 
                AB  - Glucocorticoids contribute to the increased incidence of secondary osteoporosis. Hydrogen sulfide (H2S) is a gasotransmitter and plays an essential role in bone metabolism. In this study, we investigated the therapeutic effects of H2S on glucocorticoid-induced osteoporosis (GIO). We found that dexamethasone (Dex) decreased serum H2S and two key H2S-generating enzymes in the bone marrow in vivo, cystathione b-synthase and cystathione g-lyase. Treatment of H2S-donor GYY4137 in rat significantly relieved the inhibitory effect of Dex on bone formation. Dex inhibited osteoblasts proliferation and osteogenic differentiation and decreased the expressions of the two H2S-generating enzymes. Further investigation showed that H2S was involved in Dex-mediated osteoblasts proliferation, differentiation, and apoptosis. Mechanistically, GYY4137 promoted osteoblastogenesis by activating Wnt signaling through increased production of the Wnt ligands. In comparison, the blockage of Wnt/&#x3B2;-catenin signaling pathway significantly alleviated the effect of H2S on osteoblasts. In conclusion, the restoration of H2S levels is a potential novel therapeutic approach for GIO.
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Long non-coding RNA TUG1 enhances chemosensitivity in non-small cell lung cancer by impairing microRNA-221-dependent PTEN inhibition

Shenghu Guo, Lei Zhang, Yuehua Zhang, Zheng Wu, Dongwei He, Xing Li, Zhiyu Wang,

https://doi.org/10.18632/aging.102271 pp 7553—7569

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Guo S, Zhang L, Zhang Y, Wu Z, He D, Li X, Wang Z, . Long non-coding RNA TUG1 enhances chemosensitivity in non-small cell lung cancer by impairing microRNA-221-dependent PTEN inhibition. . 11:7553-7569. https://doi.org/10.18632/aging.102271

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                TY  - JOUR
                AU  - Guo, Shenghu 
                AU  - Zhang, Lei 
                AU  - Zhang, Yuehua 
                AU  - Wu, Zheng 
                AU  - He, Dongwei 
                AU  - Li, Xing 
                AU  - Wang, Zhiyu 
                TI  - Long non-coding RNA TUG1 enhances chemosensitivity in non-small cell lung cancer by impairing microRNA-221-dependent PTEN inhibition
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102271
                DO  - 10.18632/aging.102271
                SP  - 7553
                EP  - 7569
                PY  - 
                AB  - Long non-coding RNA taurine up-regulated gene 1 (TUG1) emerges as new players in gene regulation in several cancers; however, its mechanism of action in non-small cell lung cancer (NSCLC) has not been well-studied. Herein, we determined expression pattern of TUG1 in NSCLC and further identified its effect on the chemosensitivity of NSCLC. Low expression of TUG1 was found in NSCLC tissues obtained from non-responders to platinum-based chemotherapy and reflected poor overall survival. TUG1 overexpression was shown to inhibit cell proliferation, migration, invasion, but facilitate apoptosis and autophagy in NSCLC cells resistant to cisplatin (DDP). Smaller size of tumor xenografts of DDP resistant NSCLC cells in the presence of TUG1 demonstrated enhancement of chemosensitivity by TUG1 in vivo. High expression of miR-221 and low expression of PTEN were determined in cancer tissues obtained from non-responders to platinum-based chemotherapy and reflected poor overall survival. TUG1 inhibited miR-221 that targeted PTEN, as evidenced by an elevated expression of PTEN in the presence of miR-221 or the absence of TUG1. Our present study reveals a model of enhancement of chemosensitivity that consists of TUG1, miR-221 and PTEN. Modulation of their levels may offer a new approach for improving anti-tumor efficacy for chemotherapeutic agents in NSCLC.
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Upregulation of miR-93 and inhibition of LIMK1 improve ventricular remodeling and alleviate cardiac dysfunction in rats with chronic heart failure by inhibiting RhoA/ROCK signaling pathway activation

Qian Su, Peng Zhang, Dong Yu, Zhaodi Wu, Dandan Li, Fangfang Shen, Pengfei Liao, Guizhi Yin,

https://doi.org/10.18632/aging.102272 pp 7570—7586

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Su Q, Zhang P, Yu D, Wu Z, Li D, Shen F, Liao P, Yin G, . Upregulation of miR-93 and inhibition of LIMK1 improve ventricular remodeling and alleviate cardiac dysfunction in rats with chronic heart failure by inhibiting RhoA/ROCK signaling pathway activation. . 11:7570-7586. https://doi.org/10.18632/aging.102272

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                TY  - JOUR
                AU  - Su, Qian 
                AU  - Zhang, Peng 
                AU  - Yu, Dong 
                AU  - Wu, Zhaodi 
                AU  - Li, Dandan 
                AU  - Shen, Fangfang 
                AU  - Liao, Pengfei 
                AU  - Yin, Guizhi 
                TI  - Upregulation of miR-93 and inhibition of LIMK1 improve ventricular remodeling and alleviate cardiac dysfunction in rats with chronic heart failure by inhibiting RhoA/ROCK signaling pathway activation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102272
                DO  - 10.18632/aging.102272
                SP  - 7570
                EP  - 7586
                PY  - 
                AB  - Objective: There are some researches about the role of microRNA (miRNA) in chronic heart failure (CHF) were performed, but the study about miR-93&#x2019;s function in CHF is scarcely investigated. Thus, we determined to probe into the effects of miR-93 in rats with CHF by targeting LIMK1 through regulating RhoA/ROCK pathway.Results: We found increased LIMK1 and decreased miR-93 in CHF rats, and up-regulation of miR-93 inhibited LIMK1, RhoA and ROCK1 expression in CHF rats. Up-regulation of miR-93 or inhibition of LIMK1 decreased oxidative stress, inflammatory factors, as well as apoptosis-related indicators in CHF rats. LIMK1 was confirmed as a direct target gene of miR-93.Conclusion: Our study provides evidence that upregulated miR-93 and downregulated LIMK1 improve ventricular remodeling and reduce cardiac dysfunction in CHF rats by inhibiting RhoA/ROCK signaling pathway activation.Methods: First, rat models of CHF were established by aortic coarctation, and the rats were injected with miR-93 mimics, LIMK1-siRNA or overexpressed-LIMK1. Then expression of miR-93, LIMK1, RhoA, and ROCK1 expression in myocardial tissues were detected, after which indices of cardiac ultrasound, hemodynamics, and oxidative stress, inflammatory factors, apoptosis-related indicators were detected via a series of assays. Finally, the targeting relationship of miR-93 and LIMK1 was verified.
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Attenuated activation of the unfolded protein response following exercise in skeletal muscle of older adults

Corey R. Hart, Zachary C. Ryan, Kyle T. Pfaffenbach, Surendra Dasari, Mojtaba Parvizi, Antigoni Z. Lalia, Ian R. Lanza,

https://doi.org/10.18632/aging.102273 pp 7587—7604

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Hart CR, Ryan ZC, Pfaffenbach KT, Dasari S, Parvizi M, Lalia AZ, Lanza IR, . Attenuated activation of the unfolded protein response following exercise in skeletal muscle of older adults. . 11:7587-7604. https://doi.org/10.18632/aging.102273

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                TY  - JOUR
                AU  - Hart, Corey R. 
                AU  - Ryan, Zachary C. 
                AU  - Pfaffenbach, Kyle T. 
                AU  - Dasari, Surendra 
                AU  - Parvizi, Mojtaba 
                AU  - Lalia, Antigoni Z. 
                AU  - Lanza, Ian R. 
                TI  - Attenuated activation of the unfolded protein response following exercise in skeletal muscle of older adults
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102273
                DO  - 10.18632/aging.102273
                SP  - 7587
                EP  - 7604
                PY  - 
                AB  - Sarcopenia is linked with impaired adaptive responses to exercise in aging skeletal muscle. The unfolded protein response (UPR) is an important intramyocellular molecular response pathway that is activated by exercise. The influence of age on skeletal muscle adaptive UPR in response to exercise, and the relationship to other key exercise-responsive regulatory pathways is not well-understood. We evaluated age-related changes in transcriptional markers of UPR activation following a single bout of resistance exercise in 12 young (27 &#xB1; 5yrs) and 12 older (75 &#xB1; 5yrs) healthy men and women. At baseline, there were modest differences in expression of UPR-related genes in young and older adults. Following exercise, transcriptional markers of UPR pathway activation were attenuated in older adults compared to young based on specific salient UPR-related genes and gene set enrichment analysis. The coordination of post-exercise transcriptional patterns between the UPR pathway, p53/p21 axis of autophagy, and satellite cell differentiation were less evident in older compared to young adults. In conclusion, transcriptomic analysis revealed an age-related decline in the adaptive UPR transcriptional response following a single bout of exercise that could contribute to impaired exercise responsiveness with age.
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Adherence to a healthy lifestyle counteracts the negative effects of risk factors on all-cause mortality in the oldest-old

Zhi Cao, Rui Wang, Yangyang Cheng, Hongxi Yang, Shu Li, Li Sun, Weili Xu, Yaogang Wang,

https://doi.org/10.18632/aging.102274 pp 7605—7619

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Cao Z, Wang R, Cheng Y, Yang H, Li S, Sun L, Xu W, Wang Y, . Adherence to a healthy lifestyle counteracts the negative effects of risk factors on all-cause mortality in the oldest-old. . 11:7605-7619. https://doi.org/10.18632/aging.102274

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                TY  - JOUR
                AU  - Cao, Zhi 
                AU  - Wang, Rui 
                AU  - Cheng, Yangyang 
                AU  - Yang, Hongxi 
                AU  - Li, Shu 
                AU  - Sun, Li 
                AU  - Xu, Weili 
                AU  - Wang, Yaogang 
                TI  - Adherence to a healthy lifestyle counteracts the negative effects of risk factors on all-cause mortality in the oldest-old
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102274
                DO  - 10.18632/aging.102274
                SP  - 7605
                EP  - 7619
                PY  - 
                AB  - In the study, we examined the extent to which the harmful effects of risk factors on all-cause mortality can be counteracted by healthy lifestyle practices in the oldest-old (80 years of age and older). A total of 17,660 oldest-old from China were followed up for up to 10 years. The data were analyzed using the Cox proportional hazard model with adjustment for potential confounders. We found that having a rural residence, not being married, having lower economic status, physical disability, impaired cognitive function, or comorbidity were all associated with an elevated risk of mortality. Using these factors, we computed a weighted &#x201C;risk score.&#x201D; Because never smoking, never drinking, doing physical exercise, having an ideal diet, and a normal weight were independently associated with lower mortality, we also combined them to compute a weighted &#x201C;protection score.&#x201D; Both scores were divided into lowest, middle, and highest groups using their tertiles. In joint effect analyses, participants with the combined highest-risk score and lowest-protection score profile had a nearly threefold higher joint death risk. These analyses show that adherence to a healthy lifestyle counteracts the negative effect of risk factors on all-cause mortality in the oldest-old by more than 20%.
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Co-expression network analysis identified hub genes critical to triglyceride and free fatty acid metabolism as key regulators of age-related vascular dysfunction in mice

Huimin Li, Xinhui Wang, Xinyue Lu, Hongxin Zhu, Sheng Li, Shiwei Duan, Xinzhi Zhao, Fuquan Zhang, Gil Alterovitz, Fudi Wang, Qiang Li, Xiao-Li Tian, Mingqing Xu,

https://doi.org/10.18632/aging.102275 pp 7620—7638

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Li H, Wang X, Lu X, Zhu H, Li S, Duan S, Zhao X, Zhang F, Alterovitz G, Wang F, Li Q, Tian X, Xu M, . Co-expression network analysis identified hub genes critical to triglyceride and free fatty acid metabolism as key regulators of age-related vascular dysfunction in mice. . 11:7620-7638. https://doi.org/10.18632/aging.102275

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                TY  - JOUR
                AU  - Li, Huimin 
                AU  - Wang, Xinhui 
                AU  - Lu, Xinyue 
                AU  - Zhu, Hongxin 
                AU  - Li, Sheng 
                AU  - Duan, Shiwei 
                AU  - Zhao, Xinzhi 
                AU  - Zhang, Fuquan 
                AU  - Alterovitz, Gil 
                AU  - Wang, Fudi 
                AU  - Li, Qiang 
                AU  - Tian, Xiao-Li 
                AU  - Xu, Mingqing 
                TI  - Co-expression network analysis identified hub genes critical to triglyceride and free fatty acid metabolism as key regulators of age-related vascular dysfunction in mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102275
                DO  - 10.18632/aging.102275
                SP  - 7620
                EP  - 7638
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Huimin 
                AU  - Wang, Xinhui 
                AU  - Lu, Xinyue 
                AU  - Zhu, Hongxin 
                AU  - Li, Sheng 
                AU  - Duan, Shiwei 
                AU  - Zhao, Xinzhi 
                AU  - Zhang, Fuquan 
                AU  - Alterovitz, Gil 
                AU  - Wang, Fudi 
                AU  - Li, Qiang 
                AU  - Tian, Xiao-Li 
                AU  - Xu, Mingqing 
                TI  - Co-expression network analysis identified hub genes critical to triglyceride and free fatty acid metabolism as key regulators of age-related vascular dysfunction in mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102275
                DO  - 10.18632/aging.102275
                SP  - 7620
                EP  - 7638
                PY  - 
                AB  - Background: Aging has often been linked to age-related vascular disorders. The elucidation of the putative genes and pathways underlying vascular aging likely provides useful insights into vascular diseases at advanced ages. Transcriptional regulatory network analysis is the key to describing genetic interactions between molecular regulators and their target gene transcriptionally changed during vascular aging.Results: A total of 469 differentially expressed genes were parsed into 6 modules. Among the incorporated sample traits, the most significant module related to vascular aging was associated with triglyceride and enriched with biological terms like proteolysis, blood circulation, and circulatory system process. The module associated with triglyceride was preserved in an independent microarray dataset, indicating the robustness of the identified vascular aging-related subnetwork. Additionally, Enpp5, Fez1, Kif1a, F3, H2-Q7, and their interacting miRNAs mmu-miR-449a, mmu-miR-449c, mmu-miR-34c, mmu-miR-34b-5p, mmu-miR-15a, and mmu-let-7, exhibited the most connectivity with external lipid-related traits. Transcriptional alterations of the hub genes Enpp5, Fez1, Kif1a, and F3, and the interacting microRNAs mmu-miR-34c, mmu-miR-34b-5p, mmu-let-7, mmu-miR-449a, and mmu-miR-449c were confirmed.Conclusion: Our findings demonstrate that triglyceride and free fatty acid-related genes are key regulators of age-related vascular dysfunction in mice and show that the hub genes for Enpp5, Fez1, Kif1a, and F3 as well as their interacting miRNAs mmu-miR-34c, mmu-miR-34b-5p, mmu-let-7, mmu-miR-449a, and mmu-miR-449c, could serve as potential biomarkers in vascular aging.Methods: The microarray gene expression profiles of aorta samples from 6-month old mice (n=6) and 20-month old mice (n=6) were processed to identify nominal differentially expressed genes. These nominal differentially expressed genes were subjected to a weighted gene co-expression network analysis. A network-driven integrative analysis with microRNAs and transcription factors was performed to define significant modules and underlying regulatory pathways associated with vascular aging, and module preservation test was conducted to validate the age-related modules based on an independent microarray gene expression dataset in mice aorta samples including three 32-week old wild-type mice (around 6-month old) and three 78-week old wild-type mice (around 20-month old). Gene ontology and protein-protein interaction analyses were conducted to determine the hub genes as potential biomarkers in the progress of vascular aging. The hub genes were further validated with quantitative real-time polymerase chain reaction in aorta samples from 20 young (6-month old) mice and 20 old (20-month old) mice.
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miR-125a-5p inhibits tumorigenesis in hepatocellular carcinoma

Xin Xu, Yuquan Tao, Yongjie Niu, Zhixian Wang, Congcong Zhang, Yongchun Yu, Lifang Ma,

https://doi.org/10.18632/aging.102276 pp 7639—7662

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Xu X, Tao Y, Niu Y, Wang Z, Zhang C, Yu Y, Ma L, . miR-125a-5p inhibits tumorigenesis in hepatocellular carcinoma. . 11:7639-7662. https://doi.org/10.18632/aging.102276

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                TY  - JOUR
                AU  - Xu, Xin 
                AU  - Tao, Yuquan 
                AU  - Niu, Yongjie 
                AU  - Wang, Zhixian 
                AU  - Zhang, Congcong 
                AU  - Yu, Yongchun 
                AU  - Ma, Lifang 
                TI  - miR-125a-5p inhibits tumorigenesis in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102276
                DO  - 10.18632/aging.102276
                SP  - 7639
                EP  - 7662
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is one of the most prevalent and deadly cancers world-wide. miR-125a-5p is a tumor suppressor in HCC and other cancers, but its mechanisms of action during HCC tumorigenesis remain largely unknown. In this study, we found that miR-125a-5p expression was significantly lower in HCC tissues and cell lines than matched normal tissues and liver cells. miR-125a-5p overexpression inhibited HCC cell proliferation and induced apoptosis in vitro and in vivo, while miR-125a-5p knockdown had the opposite effects. In addition, PTPN1 and MAP3K11 were identified as targets of miR-125a-5p. Knocking down PTPN1 and MAP3K11 activated the JNK MAPK signaling pathway to suppress HCC cell proliferation and induce apoptosis. Our findings suggest that miR-125a-5p may be a useful therapeutic target for treatment of HCC patients.
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Association between promoter DNA methylation and gene expression in the pathogenesis of ischemic stroke

Guo-Xiong Deng, Ning Xu, Qi Huang, Jin-Yue Tan, Zhao Zhang, Xian-Feng Li, Jin-Ru Wei,

https://doi.org/10.18632/aging.102278 pp 7663—7677

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Deng G, Xu N, Huang Q, Tan J, Zhang Z, Li X, Wei J, . Association between promoter DNA methylation and gene expression in the pathogenesis of ischemic stroke. . 11:7663-7677. https://doi.org/10.18632/aging.102278

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                TY  - JOUR
                AU  - Deng, Guo-Xiong 
                AU  - Xu, Ning 
                AU  - Huang, Qi 
                AU  - Tan, Jin-Yue 
                AU  - Zhang, Zhao 
                AU  - Li, Xian-Feng 
                AU  - Wei, Jin-Ru 
                TI  - Association between promoter DNA methylation and gene expression in the pathogenesis of ischemic stroke
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102278
                DO  - 10.18632/aging.102278
                SP  - 7663
                EP  - 7677
                PY  - 
                AB  - To assess DNA methylation sites as well as gene expression related to ischemic stroke (IS) and comprehensively reveal their correlation and possible pathological mechanisms, we implemented (1) genome-wide DNA methylation profiling from the GEO repository related to IS with and without symptoms; (2) identification of differentially methylation positions (DMPs) and genes (DMGs), functional enrichment analysis along with DMG regulatory network construction; (3) validation tests of 2 differential methylation positions of interest as well as analogous gene expression in other datasets and in IS patients and controls; and (4) correlation analysis of DNA methylation and mRNA expression data. In total, 870 DMPs were physically located within 693 DMGs. After disease ontology (DO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, gene ontology (GO), protein-protein interaction (PPI) network construction as well as module analysis, HLA-DRB1 and HLA-DQB1 were identified. Their expression was validated in 4 other datasets but was significant in only 1, and the expression was lower in the IS group (P &lt; 0.05). After validation in IS patients and controls, we found that these two genes showed more hypermethylation and lower expression levels in the IS group (P &lt; 0.001). The methylation of genes was negatively associated with their expression (P &lt; 0.05). The current study recognized a connection among DNA methylation and gene expression and emphasized the prominence of HLA-DRB1 and HLA-DQB1 in IS pathogenesis.
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Long noncoding RNA TTN-AS1 enhances the malignant characteristics of osteosarcoma by acting as a competing endogenous RNA on microRNA-376a thereby upregulating dickkopf-1

Shenglong Li, Fei Liu, Yi Pei, Wei Wang, Ke Zheng, Xiaojing Zhang,

https://doi.org/10.18632/aging.102280 pp 7678—7693

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Li S, Liu F, Pei Y, Wang W, Zheng K, Zhang X, . Long noncoding RNA TTN-AS1 enhances the malignant characteristics of osteosarcoma by acting as a competing endogenous RNA on microRNA-376a thereby upregulating dickkopf-1. . 11:7678-7693. https://doi.org/10.18632/aging.102280

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 TY - JOUR
 AU - Li, Shenglong 
 AU - Liu, Fei 
 AU - Pei, Yi 
 AU - Wang, Wei 
 AU - Zheng, Ke 
 AU - Zhang, Xiaojing 
 TI - Long noncoding RNA TTN-AS1 enhances the malignant characteristics of osteosarcoma by acting as a competing endogenous RNA on microRNA-376a thereby upregulating dickkopf-1
 JO - 
 JA - 
 VL - 11
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102280
 DO - 10.18632/aging.102280
 SP - 7678
 EP - 7693
 PY - 
 AB - The expression levels and detailed functions of TTN-AS1 in osteosarcoma (OS) have not yet been explored. This study aimed to measure TTN-AS1 expression in OS tissues and cell lines, investigate its specific roles in the aggressive characteristics of OS cells in vitro and in vivo, and elucidate the regulatory mechanisms of TTN-AS1 action. TTN-AS1 expression was high in OS tissue samples and cell lines; TTN-AS1 overexpression correlated with the clinical stage, distant metastasis, and shorter overall survival of the patients. A TTN-AS1 knockdown inhibited OS cell proliferation, migration, and invasion and induced apoptosis in vitro and slowed tumor growth in vivo. Mechanism investigation revealed that TTN-AS1 acts as a competing endogenous RNA on microRNA-376a-3p (miR-376a) in OS cells. Dickkopf-1 (DKK1) mRNA was identified as a direct target of miR-376a in OS cells. Resumption of DKK1 expression reversed the tumor-suppressive activities of miR-376a overexpression in OS cells. The knockdown of miR-376a counteracted the reduction in the malignant characteristics of OS cells by the downregulation of TTN-AS1. In conclusion, TTN-AS1 functions as a competing endogenous RNA targeting miR-376a and increases the malignancy of OS cells in vitro and in vivo by upregulating DKK1.
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Circulating glucuronic acid predicts healthspan and longevity in humans and mice

Andrew Ho, Jonah Sinick, Tõnu Esko, Krista Fischer, Cristina Menni, Jonas Zierer, Maria Matey-Hernandez, Kristen Fortney, Eric K. Morgen,

https://doi.org/10.18632/aging.102281 pp 7694—7706

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Ho A, Sinick J, Esko T, Fischer K, Menni C, Zierer J, Matey-Hernandez M, Fortney K, Morgen EK, . Circulating glucuronic acid predicts healthspan and longevity in humans and mice. . 11:7694-7706. https://doi.org/10.18632/aging.102281

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                TY  - JOUR
                AU  - Ho, Andrew 
                AU  - Sinick, Jonah 
                AU  - Esko, Tõnu 
                AU  - Fischer, Krista 
                AU  - Menni, Cristina 
                AU  - Zierer, Jonas 
                AU  - Matey-Hernandez, Maria 
                AU  - Fortney, Kristen 
                AU  - Morgen, Eric K. 
                TI  - Circulating glucuronic acid predicts healthspan and longevity in humans and mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102281
                DO  - 10.18632/aging.102281
                SP  - 7694
                EP  - 7706
                PY  - 
                AB  - Glucuronic acid is a metabolite of glucose that is involved in the detoxification of xenobiotic compounds and the structure/remodeling of the extracellular matrix. We report for the first time that circulating glucuronic acid is a robust biomarker of mortality that is conserved across species. We find that glucuronic acid levels are significant predictors of all-cause mortality in three population-based cohorts from different countries with 4-20 years of follow-up (HR=1.44, p=2.9&#xD7;10-6 in the discovery cohort; HR=1.13, p=0.032 and HR=1.25, p=0.017, respectively in the replication cohorts), as well as in a longitudinal study of genetically heterogenous mice (HR=1.29, p=0.018). Additionally, we find that glucuronic acid levels increase with age and predict future healthspan-related outcomes. Together, these results demonstrate glucuronic acid as a robust biomarker of longevity and healthspan.
                ER  -

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Single-cell RNA-seq reveals RAD51AP1 as a potent mediator of EGFRvIII in human glioblastomas

Qixue Wang, Yanli Tan, Chuan Fang, Junhu Zhou, Yunfei Wang, Kai Zhao, Weili Jin, Ye Wu, Xiaomin Liu, Xing Liu, Chunsheng Kang,

https://doi.org/10.18632/aging.102282 pp 7707—7722

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Wang Q, Tan Y, Fang C, Zhou J, Wang Y, Zhao K, Jin W, Wu Y, Liu X, Liu X, Kang C, . Single-cell RNA-seq reveals RAD51AP1 as a potent mediator of EGFRvIII in human glioblastomas. . 11:7707-7722. https://doi.org/10.18632/aging.102282

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                TY  - JOUR
                AU  - Wang, Qixue 
                AU  - Tan, Yanli 
                AU  - Fang, Chuan 
                AU  - Zhou, Junhu 
                AU  - Wang, Yunfei 
                AU  - Zhao, Kai 
                AU  - Jin, Weili 
                AU  - Wu, Ye 
                AU  - Liu, Xiaomin 
                AU  - Liu, Xing 
                AU  - Kang, Chunsheng 
                TI  - Single-cell RNA-seq reveals RAD51AP1 as a potent mediator of EGFRvIII in human glioblastomas
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102282
                DO  - 10.18632/aging.102282
                SP  - 7707
                EP  - 7722
                PY  - 
                AB  - Recent advances in single-cell RNA sequencing (scRNA-seq) have endowed researchers with the ability to detect and analyze the transcriptomes of individual cancer cells. In the present study, 16,128 tumor cells from EGFR wild-type and EGFRvIII mutant cells were profiled by scRNA-seq. Analyses of scRNA-seq data from both U87MG and U87MG-EGFRvIII libraries revealed inherent heterogeneity in gene expression and biological processes. The cells stably expressing EGFRvIII showed enhanced transcriptional activities and a relatively homogeneous pattern, which manifested as less diverse distributions, gene expression levels and functional annotations compared with those of cells expressing the nonmutated version. Moreover, the differentially expressed genes between the U87MG and U87MG-EGFRvIII groups were mainly enriched in DNA replication, DNA repair and angiogenesis. We compared scRNA-seq data with bulk RNA-seq and EGFRvIII xenograft RNA-seq data. RAD51AP1 was shown to be upregulated in all three databases. Further analysis of RAD51AP1 revealed that it is an independent prognostic factor of glioma. Knocking down RAD51AP1 significantly inhibited tumor volume in an intracranial EGFRvIII-positive GBM model and prolonged survival time. Collectively, our microfluidic-based scRNA-seq driven by a single genetic event revealed a previously unappreciated implication of EGFRvIII in the heterogeneity of GBM and identified RAD51AP1 as an oncogene in glioma.
                ER  -

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Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1

Yuluo Rong, Wei Liu, Chengtang Lv, Jiaxing Wang, Yongjun Luo, Dongdong Jiang, Linwei Li, Zheng Zhou, Wei Zhou, Qingqing Li, Guoyong Yin, Lipeng Yu, Jin Fan, Weihua Cai,

https://doi.org/10.18632/aging.102283 pp 7723—7745

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Rong Y, Liu W, Lv C, Wang J, Luo Y, Jiang D, Li L, Zhou Z, Zhou W, Li Q, Yin G, Yu L, Fan J, et al, . Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1. . 11:7723-7745. https://doi.org/10.18632/aging.102283

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                TY  - JOUR
                AU  - Rong, Yuluo 
                AU  - Liu, Wei 
                AU  - Lv, Chengtang 
                AU  - Wang, Jiaxing 
                AU  - Luo, Yongjun 
                AU  - Jiang, Dongdong 
                AU  - Li, Linwei 
                AU  - Zhou, Zheng 
                AU  - Zhou, Wei 
                AU  - Li, Qingqing 
                AU  - Yin, Guoyong 
                AU  - Yu, Lipeng 
                AU  - Fan, Jin 
                AU  - Cai, Weihua 
                TI  - Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102283
                DO  - 10.18632/aging.102283
                SP  - 7723
                EP  - 7745
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Rong, Yuluo 
                AU  - Liu, Wei 
                AU  - Lv, Chengtang 
                AU  - Wang, Jiaxing 
                AU  - Luo, Yongjun 
                AU  - Jiang, Dongdong 
                AU  - Li, Linwei 
                AU  - Zhou, Zheng 
                AU  - Zhou, Wei 
                AU  - Li, Qingqing 
                AU  - Yin, Guoyong 
                AU  - Yu, Lipeng 
                AU  - Fan, Jin 
                AU  - Cai, Weihua 
                TI  - Neural stem cell small extracellular vesicle-based delivery of 14-3-3t reduces apoptosis and neuroinflammation following traumatic spinal cord injury by enhancing autophagy by targeting Beclin-1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102283
                DO  - 10.18632/aging.102283
                SP  - 7723
                EP  - 7745
                PY  - 
                AB  - Neural stem cell-derived small extracellular vesicles (NSC-sEVs) play an important role in the repair of tissue damage. Our previous in vitro and in vivo studies found that preconditioning with NSC-sEVs promoted the recovery of functional behaviors following spinal cord injury by activating autophagy. However, the underlying mechanisms for such observations remain unclear. In this study, we further explored the mechanisms by which NSC-sEVs repair spinal cord injury via autophagy. We found that NSC-sEVs contain 14-3-3t protein, of which the overexpression or knockdown enhanced and decreased autophagy, respectively. In addition, 14-3-3t overexpression enhanced the anti-apoptotic and anti-inflammatory effects of NSC-sEVs, further promoting functional behavior recovery following spinal cord injury. The overexpression of 14-3-3t was used to further validate the in vivo results through a series of in vitro experiments. Conversely, knockdown of 14-3-3t attenuated the anti-apoptotic and anti-inflammatory effects of NSC-sEVs. Further studies also confirmed that NSC-sEVs increased Beclin-1 expression, with which 14-3-3t interacted and promoted its localization to autophagosome precursors. In this study, we found that NSC-sEVs deliver 14-3-3t, which interacts with Beclin-1 to activate autophagy. Our results indicate that 14-3-3t acts via a newly-discovered mechanism for the activation of autophagy by NSC-sEVs.
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Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging

Livia López-Noriega, Vivian Capilla-González, Nadia Cobo-Vuilleumier, Eugenia Martin-Vazquez, Petra Isabel Lorenzo, Enrique Martinez-Force, Mario Soriano-Navarro, María García-Fernández, Silvana Yanina Romero-Zerbo, Francisco Javier Bermúdez-Silva, Irene Díaz-Contreras, Ana Sánchez-Cuesta, Carlos Santos-Ocaña, Abdelkrim Hmadcha, Bernat Soria, Franz Martín, Benoit Raymond Gauthier, Alejandro Martin-Montalvo,

https://doi.org/10.18632/aging.102285 pp 7746—7779

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López-Noriega L, Capilla-González V, Cobo-Vuilleumier N, Martin-Vazquez E, Lorenzo PI, Martinez-Force E, Soriano-Navarro M, García-Fernández M, Romero-Zerbo SY, Bermúdez-Silva FJ, Díaz-Contreras I, Sánchez-Cuesta A, Santos-Ocaña C, et al, . Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging. . 11:7746-7779. https://doi.org/10.18632/aging.102285

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                TY  - JOUR
                AU  - López-Noriega, Livia 
                AU  - Capilla-González, Vivian 
                AU  - Cobo-Vuilleumier, Nadia 
                AU  - Martin-Vazquez, Eugenia 
                AU  - Lorenzo, Petra Isabel 
                AU  - Martinez-Force, Enrique 
                AU  - Soriano-Navarro, Mario 
                AU  - García-Fernández, María 
                AU  - Romero-Zerbo, Silvana Yanina 
                AU  - Bermúdez-Silva, Francisco Javier 
                AU  - Díaz-Contreras, Irene 
                AU  - Sánchez-Cuesta, Ana 
                AU  - Santos-Ocaña, Carlos 
                AU  - Hmadcha, Abdelkrim 
                AU  - Soria, Bernat 
                AU  - Martín, Franz 
                AU  - Gauthier, Benoit Raymond 
                AU  - Martin-Montalvo, Alejandro 
                TI  - Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102285
                DO  - 10.18632/aging.102285
                SP  - 7746
                EP  - 7779
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - López-Noriega, Livia 
                AU  - Capilla-González, Vivian 
                AU  - Cobo-Vuilleumier, Nadia 
                AU  - Martin-Vazquez, Eugenia 
                AU  - Lorenzo, Petra Isabel 
                AU  - Martinez-Force, Enrique 
                AU  - Soriano-Navarro, Mario 
                AU  - García-Fernández, María 
                AU  - Romero-Zerbo, Silvana Yanina 
                AU  - Bermúdez-Silva, Francisco Javier 
                AU  - Díaz-Contreras, Irene 
                AU  - Sánchez-Cuesta, Ana 
                AU  - Santos-Ocaña, Carlos 
                AU  - Hmadcha, Abdelkrim 
                AU  - Soria, Bernat 
                AU  - Martín, Franz 
                AU  - Gauthier, Benoit Raymond 
                AU  - Martin-Montalvo, Alejandro 
                TI  - Inadequate control of thyroid hormones sensitizes to hepatocarcinogenesis and unhealthy aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102285
                DO  - 10.18632/aging.102285
                SP  - 7746
                EP  - 7779
                PY  - 
                AB  - An inverse correlation between thyroid hormone levels and longevity has been reported in several species and reduced thyroid hormone levels have been proposed as a biomarker for healthy aging and metabolic fitness. However, hypothyroidism is a medical condition associated with compromised health and reduced life expectancy. Herein, we show, using wild-type and the Pax8 ablated model of hypothyroidism in mice, that hyperthyroidism and severe hypothyroidism are associated with an overall unhealthy status and shorter lifespan. Mild hypothyroid Pax8 +/- mice were heavier and displayed insulin resistance, hepatic steatosis and increased prevalence of liver cancer yet had normal lifespan. These pathophysiological conditions were precipitated by hepatic mitochondrial dysfunction and oxidative damage accumulation. These findings indicate that individuals carrying mutations on PAX8 may be susceptible to develop liver cancer and/or diabetes and raise concerns regarding the development of interventions aiming to modulate thyroid hormones to promote healthy aging or lifespan in mammals.
                ER  -

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Sulfated polysaccharide of Sepiella maindroni ink targets Akt and overcomes resistance to the FGFR inhibitor AZD4547 in bladder cancer

Liping Shan, Wei Liu, Yunhong Zhan,

https://doi.org/10.18632/aging.102286 pp 7780—7795

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Shan L, Liu W, Zhan Y, . Sulfated polysaccharide of Sepiella maindroni ink targets Akt and overcomes resistance to the FGFR inhibitor AZD4547 in bladder cancer. . 11:7780-7795. https://doi.org/10.18632/aging.102286

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Provider: 
 TY - JOUR
 AU - Shan, Liping 
 AU - Liu, Wei 
 AU - Zhan, Yunhong 
 TI - Sulfated polysaccharide of Sepiella maindroni ink targets Akt and overcomes resistance to the FGFR inhibitor AZD4547 in bladder cancer
 JO - 
 JA - 
 VL - 11
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102286
 DO - 10.18632/aging.102286
 SP - 7780
 EP - 7795
 PY - 
 AB - Rapid appearance of resistance to fibroblast growth factor receptor (FGFR) inhibitors hampers targeted regimens in bladder cancer. In the present study, we evaluated whether SIP-SII, a sulphated derivative of the polysaccharide in Sepiella maindroni (spineless cuttlefish) ink used in traditional Chinese medicine, could attenuate resistance to FGFR inhibition in bladder cancer cells. In vitro assays indicated that SIP-SII reduced cell viability and migration, restricted cell cycle progression, and increased apoptosis in parallel with decreased AKT phosphorylation and downregulation of CDK4, MMP2, and Bcl-2 in RT112 and JMSU1 cells. Synergistic effects on cell viability were observed when SIP-SII was combined with the small-molecule FGFR inhibitor AZD4547. Specific Akt targeting by SIP-SII was suggested by the fact that neither Akt knockdown nor the selective PI3K inhibitor BKM120 enhanced the inhibitory effects of SIP-II, while expression of a constitutively active Akt mutant rescued SIP-SII effects. Furthermore, subcutaneous transplantation of RT112 xenografts confirmed the superiority and tolerability of combined SIP-SII and AZD4547 administration over monotherapy regimens. The present study thus provides pre-clinical evidence of the ability of SIP-SII to improve FGFR-targeted therapies for bladder cancer by inhibiting Akt.
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Up-regulation of lysophosphatidylcholine acyltransferase 1 (LPCAT1) is linked to poor prognosis in breast cancer

Patrick Lebok, Aurelia von Hassel, Jan Meiners, Claudia Hube-Magg, Ronald Simon, Doris Höflmayer, Andrea Hinsch, David Dum, Christoph Fraune, Cosima Göbel, Katharina Möller, Guido Sauter, Frank Jacobsen, Franziska Büscheck, Kristina Prien, Till Krech, Rainer Horst Krech, Albert von der Assen, Linn Wölber, Isabell Witzel, Barbara Schmalfeldt, Stefan Geist, Peter Paluchoswski, Christian Wilke, Uwe Heilenkötter, Luigi Terracciano, Volkmar Müller, Waldemar Wilczak, Eike Christian Burandt,

https://doi.org/10.18632/aging.102287 pp 7796—7804

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Lebok P, von Hassel A, Meiners J, Hube-Magg C, Simon R, Höflmayer D, Hinsch A, Dum D, Fraune C, Göbel C, Möller K, Sauter G, Jacobsen F, et al, . Up-regulation of lysophosphatidylcholine acyltransferase 1 (LPCAT1) is linked to poor prognosis in breast cancer. . 11:7796-7804. https://doi.org/10.18632/aging.102287

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                TY  - JOUR
                AU  - Lebok, Patrick 
                AU  - von Hassel, Aurelia 
                AU  - Meiners, Jan 
                AU  - Hube-Magg, Claudia 
                AU  - Simon, Ronald 
                AU  - Höflmayer, Doris 
                AU  - Hinsch, Andrea 
                AU  - Dum, David 
                AU  - Fraune, Christoph 
                AU  - Göbel, Cosima 
                AU  - Möller, Katharina 
                AU  - Sauter, Guido 
                AU  - Jacobsen, Frank 
                AU  - Büscheck, Franziska 
                AU  - Prien, Kristina 
                AU  - Krech, Till 
                AU  - Krech, Rainer Horst 
                AU  - von der Assen, Albert 
                AU  - Wölber, Linn 
                AU  - Witzel, Isabell 
                AU  - Schmalfeldt, Barbara 
                AU  - Geist, Stefan 
                AU  - Paluchoswski, Peter 
                AU  - Wilke, Christian 
                AU  - Heilenkötter, Uwe 
                AU  - Terracciano, Luigi 
                AU  - Müller, Volkmar 
                AU  - Wilczak, Waldemar 
                AU  - Burandt, Eike Christian 
                TI  - Up-regulation of lysophosphatidylcholine acyltransferase 1 (LPCAT1) is linked to poor prognosis in breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102287
                DO  - 10.18632/aging.102287
                SP  - 7796
                EP  - 7804
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lebok, Patrick 
                AU  - von Hassel, Aurelia 
                AU  - Meiners, Jan 
                AU  - Hube-Magg, Claudia 
                AU  - Simon, Ronald 
                AU  - Höflmayer, Doris 
                AU  - Hinsch, Andrea 
                AU  - Dum, David 
                AU  - Fraune, Christoph 
                AU  - Göbel, Cosima 
                AU  - Möller, Katharina 
                AU  - Sauter, Guido 
                AU  - Jacobsen, Frank 
                AU  - Büscheck, Franziska 
                AU  - Prien, Kristina 
                AU  - Krech, Till 
                AU  - Krech, Rainer Horst 
                AU  - von der Assen, Albert 
                AU  - Wölber, Linn 
                AU  - Witzel, Isabell 
                AU  - Schmalfeldt, Barbara 
                AU  - Geist, Stefan 
                AU  - Paluchoswski, Peter 
                AU  - Wilke, Christian 
                AU  - Heilenkötter, Uwe 
                AU  - Terracciano, Luigi 
                AU  - Müller, Volkmar 
                AU  - Wilczak, Waldemar 
                AU  - Burandt, Eike Christian 
                TI  - Up-regulation of lysophosphatidylcholine acyltransferase 1 (LPCAT1) is linked to poor prognosis in breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102287
                DO  - 10.18632/aging.102287
                SP  - 7796
                EP  - 7804
                PY  - 
                AB  - Dysregulation of lipid metabolism is common in cancer. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) has been implicated with various cancer types. Here we analyzed by immunohistochemistry its expression in 2,197 breast cancers. LPCAT1 staining was found in 97.8% of 1,774 interpretable tumors, including 48.1% with weak, 28.7% with moderate, and 14.4% with strong expression. The frequency of LPCAT1 positivity depended on the histological tumor type. Moderate or strong LPCAT1 positivity was more common in cancers of no special type (NST) (46.2%) than in lobular carcinomas (25.9%; p&lt;0.0001). Strong LPCAT1 was associated with BRE grade, tumor cell proliferation and overall survival in all cancers and in the subgroup of NST cancers (p&lt;0.0001, each). In the subset of NST cancers the prognostic effect of LPCAT1 expression was independent of pT, and BRE grade (p&lt;0.0001 each). A comparison with molecular features showed that LPCAT1 was strongly associated with estrogen receptor negativity (p&lt;0.0001), progesterone receptor negativity (p&lt;0,0001), amplification of HER2 (p&lt;0.0001) and MYC (p=0.0066), as well as deletions of PTEN (p&lt;0.0001) and CDKNA2 (p=0.0151). It is concluded that LPCAT1 overexpression is linked to adverse tumor features and poor prognosis in breast cancer. These data also highlight the important role of lipid metabolism in breast cancer biology.
                ER  -

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A novel chalcone derivative exerts anti-inflammatory and anti-oxidant effects after acute lung injury

Yuting Lin, Man Zhang, Qingdi Lu, Jingwen Xie, Jianzhang Wu, Chengshui Chen,

https://doi.org/10.18632/aging.102288 pp 7805—7816

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Lin Y, Zhang M, Lu Q, Xie J, Wu J, Chen C, . A novel chalcone derivative exerts anti-inflammatory and anti-oxidant effects after acute lung injury. . 11:7805-7816. https://doi.org/10.18632/aging.102288

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                TY  - JOUR
                AU  - Lin, Yuting 
                AU  - Zhang, Man 
                AU  - Lu, Qingdi 
                AU  - Xie, Jingwen 
                AU  - Wu, Jianzhang 
                AU  - Chen, Chengshui 
                TI  - A novel chalcone derivative exerts anti-inflammatory and anti-oxidant effects after acute lung injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102288
                DO  - 10.18632/aging.102288
                SP  - 7805
                EP  - 7816
                PY  - 
                AB  - We explored the effects of compound 33, a synthetic chalcone derivative with antioxidant activity, on lipopolysaccharide (LPS)-induced acute lung injury (ALI). Compound 33, dexamethasone or vehicle was administered intragastrically to mice 6 h before intratracheal instillation of LPS. After 24 h, the effects of compound 33 on alveolar structural damage were evaluated by assessing lung morphology and the wet/dry weight ratio. Protein and proinflammatory cytokine levels and superoxide dismutase activity were also examined in the cell free supernatant of bronchoalveolar lavage fluid. Additionally, we investigated the anti-inflammatory and antioxidant activity of compound 33 in vitro and its effects on the MAPK/NF-&#x3BA;B and Nrf2/HO-1 pathways. Pretreatment with compound 33 prevented LPS-induced structural damage, tissue edema, protein exudation, and overproduction of proinflammatory mediators. The effects of compound 33 were similar to or greater in magnitude than those of the positive control, dexamethasone. Moreover, compound 33 exerted anti-inflammatory and antioxidant effects in vitro by inhibiting the MAPK/NF-&#x3BA;B pathway and activating the Nrf2/HO-1 pathway. Compound 33 may therefore be a promising candidate treatment for ALI.
                ER  -

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PRL-3 exerts oncogenic functions in myeloid leukemia cells via aberrant dephosphorylation of stathmin and activation of STAT3 signaling

Jianping Xu, Wei Wu, Yao Tang, Yanfeng Lin, Yan Xue, Jianda Hu, Donghong Lin,

https://doi.org/10.18632/aging.102290 pp 7817—7829

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Xu J, Wu W, Tang Y, Lin Y, Xue Y, Hu J, Lin D, . PRL-3 exerts oncogenic functions in myeloid leukemia cells via aberrant dephosphorylation of stathmin and activation of STAT3 signaling. . 11:7817-7829. https://doi.org/10.18632/aging.102290

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                TY  - JOUR
                AU  - Xu, Jianping 
                AU  - Wu, Wei 
                AU  - Tang, Yao 
                AU  - Lin, Yanfeng 
                AU  - Xue, Yan 
                AU  - Hu, Jianda 
                AU  - Lin, Donghong 
                TI  - PRL-3 exerts oncogenic functions in myeloid leukemia cells via aberrant dephosphorylation of stathmin and activation of STAT3 signaling
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102290
                DO  - 10.18632/aging.102290
                SP  - 7817
                EP  - 7829
                PY  - 
                AB  - PRL-3, an oncogenic dual-specificity phosphatase, is overexpressed in 50% of acute myeloid leukemia patients. Stathmin has been identified as a downstream target of PRL-3 in colorectal cancer. However, the correlation between PRL-3 and stathmin in myeloid leukemia is unclear. In this study, we revealed the positive correlation between PRL-3 and stathmin in myeloid leukemia. Knockdown of the PRL-3 gene by shRNA reduced the expression of downstream stathmin, suppressed cell proliferation, induced G2/M arrest and cell apoptosis, and inhibited migration and invasion in myeloid leukemia cells. Moreover, our study was the first to provide evidence that silencing PRL-3 increased the phosphorylation level in Ser16, Ser25, Ser38, and Ser63 of stathmin, and in turn inhibited the STAT3 and STAT5 signaling in myeloid leukemia cells. This evidence points to a promoted role for PRL-3 in the progression of myeloid leukemia, and PRL-3 could be a possible new treatment target.
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Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death

Jinglei Liu, Lei Yao, Mingyan Zhang, Ji Jiang, Maopeng Yang, Yue Wang,

https://doi.org/10.18632/aging.102291 pp 7830—7846

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Liu J, Yao L, Zhang M, Jiang J, Yang M, Wang Y, . Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death. . 11:7830-7846. https://doi.org/10.18632/aging.102291

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                TY  - JOUR
                AU  - Liu, Jinglei 
                AU  - Yao, Lei 
                AU  - Zhang, Mingyan 
                AU  - Jiang, Ji 
                AU  - Yang, Maopeng 
                AU  - Wang, Yue 
                TI  - Downregulation of LncRNA-XIST inhibited development of non-small cell lung cancer by activating miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102291
                DO  - 10.18632/aging.102291
                SP  - 7830
                EP  - 7846
                PY  - 
                AB  - LncRNA-XIST participated in the regulation of Non-small cell lung cancer (NSCLC) progression, but the underlying mechanisms are still unclear. This study showed that LncRNA-XIST aberrantly overexpressed in either NSCLC tissues or cell lines comparing to their paired control groups. Knock-down of LncRNA-XIST promoted NSCLC cell apoptosis and inhibited cell proliferation, which were reversed by synergistically treating cells with pyroptosis inhibitor Necrosulfonamide (NSA). In addition, knock-down of LncRNA-XIST also promoted reactive oxygen species (ROS) production and NLRP3 inflammasome activation. In parallel, ROS scavenger N-acetyl cysteine (NAC) abrogated the effects of downregulated LncRNA-XIST on NSCLC cell pyroptosis. Furthermore, miR-335 was the downstream target of LncRNA-XIST and overexpressed LncRNA-XIST increased SOD2 expression levels by sponging miR-335. Mechanistically, miR-335 inhibitor reversed the effects of downregulated LncRNA-XIST on ROS levels and cell pyroptosis, which were abrogated by synergistically knocking down SOD2. Taken together, knock-down of LncRNA-XIST inhibited NSCLC progression by triggering miR-335/SOD2/ROS signal pathway mediated pyroptotic cell death.
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KLB gene polymorphism is associated with obesity and non-alcoholic fatty liver disease in the Han Chinese

Fang Ji, Ye Liu, Jun-Gui Hao, Li-Ping Wang, Ming-Jia Dai, Gui-Fang Shen, Xue-Bing Yan,

https://doi.org/10.18632/aging.102293 pp 7847—7858

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Ji F, Liu Y, Hao J, Wang L, Dai M, Shen G, Yan X, . KLB gene polymorphism is associated with obesity and non-alcoholic fatty liver disease in the Han Chinese. . 11:7847-7858. https://doi.org/10.18632/aging.102293

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Provider: 
 TY - JOUR
 AU - Ji, Fang 
 AU - Liu, Ye 
 AU - Hao, Jun-Gui 
 AU - Wang, Li-Ping 
 AU - Dai, Ming-Jia 
 AU - Shen, Gui-Fang 
 AU - Yan, Xue-Bing 
 TI - KLB gene polymorphism is associated with obesity and non-alcoholic fatty liver disease in the Han Chinese
 JO - 
 JA - 
 VL - 11
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102293
 DO - 10.18632/aging.102293
 SP - 7847
 EP - 7858
 PY - 
 AB - Klotho beta (KLB) mediates binding of fibroblast growth factor (FGF) 21 to the FGF receptor (FGFR). FGF21-KLB-FGFR signaling regulates multiple metabolic systems in the liver, and we hypothesized that FGF21, KLB and FGFR single-nucleotide polymorphisms (SNPs) are involved in hepatic lipid accumulation. The SNPs were detected in 1688 individuals divided into four groups: non-obese without non-alcoholic fatty liver disease (NAFLD), obese without NAFLD, non-obese with NAFLD, and obese with NAFLD. The A-allele of KLB SNP rs7670903 correlated with higher body mass index (P = 0.0005), and the A-allele frequency was higher in the obese than non-obese group (P = 0.003). The G-allele frequency of KLB rs7674434 and T-allele frequency of rs12152703 were higher in the obese with NAFLD than obese without NAFLD group (P = 0.004 and P = 0.006), but the genotype distribution between two non-obese groups did not differ. KLB rs7674434 and rs12152703 had associations with alanine aminotransferase (ALT) (P = 0.03 and P = 0.04, respectively) and gamma-glutamyltransferase (P = 0.03 and P = 0.02, respectively) levels in all subjects, but the associations were especially strong with ALT in the NAFLD group (P = 0.005 and P = 0.008, respectively). These findings suggest that KLB SNPs are related to obesity and hepatic inflammation and that they may be involved in the pathogenesis of NAFLD.
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Up regulation of Rho-associated coiled-coil containing kinase1 (ROCK1) is associated with genetic instability and poor prognosis in prostate cancer

Stefan Steurer, Benjamin Hager, Franziska Büscheck, Doris Höflmayer, Maria Christina Tsourlakis, Sarah Minner, Till S. Clauditz, Claudia Hube-Magg, Andreas M. Luebke, Ronald Simon, Jakob R. Izbicki, Eike Burandt, Guido Sauter, Christoph Fraune, Sören Weidemann, Thorsten Schlomm, Hans Heinzer, Alexander Haese, Markus Graefen, Hartwig Huland, Asmus Heumann,

https://doi.org/10.18632/aging.102294 pp 7859—7879

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Steurer S, Hager B, Büscheck F, Höflmayer D, Tsourlakis MC, Minner S, Clauditz TS, Hube-Magg C, Luebke AM, Simon R, Izbicki JR, Burandt E, Sauter G, et al, . Up regulation of Rho-associated coiled-coil containing kinase1 (ROCK1) is associated with genetic instability and poor prognosis in prostate cancer. . 11:7859-7879. https://doi.org/10.18632/aging.102294

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                TY  - JOUR
                AU  - Steurer, Stefan 
                AU  - Hager, Benjamin 
                AU  - Büscheck, Franziska 
                AU  - Höflmayer, Doris 
                AU  - Tsourlakis, Maria Christina 
                AU  - Minner, Sarah 
                AU  - Clauditz, Till S. 
                AU  - Hube-Magg, Claudia 
                AU  - Luebke, Andreas M. 
                AU  - Simon, Ronald 
                AU  - Izbicki, Jakob R. 
                AU  - Burandt, Eike 
                AU  - Sauter, Guido 
                AU  - Fraune, Christoph 
                AU  - Weidemann, Sören 
                AU  - Schlomm, Thorsten 
                AU  - Heinzer, Hans 
                AU  - Haese, Alexander 
                AU  - Graefen, Markus 
                AU  - Huland, Hartwig 
                AU  - Heumann, Asmus 
                TI  - Up regulation of Rho-associated coiled-coil containing kinase1 (ROCK1) is associated with genetic instability and poor prognosis in prostate cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102294
                DO  - 10.18632/aging.102294
                SP  - 7859
                EP  - 7879
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Steurer, Stefan 
                AU  - Hager, Benjamin 
                AU  - Büscheck, Franziska 
                AU  - Höflmayer, Doris 
                AU  - Tsourlakis, Maria Christina 
                AU  - Minner, Sarah 
                AU  - Clauditz, Till S. 
                AU  - Hube-Magg, Claudia 
                AU  - Luebke, Andreas M. 
                AU  - Simon, Ronald 
                AU  - Izbicki, Jakob R. 
                AU  - Burandt, Eike 
                AU  - Sauter, Guido 
                AU  - Fraune, Christoph 
                AU  - Weidemann, Sören 
                AU  - Schlomm, Thorsten 
                AU  - Heinzer, Hans 
                AU  - Haese, Alexander 
                AU  - Graefen, Markus 
                AU  - Huland, Hartwig 
                AU  - Heumann, Asmus 
                TI  - Up regulation of Rho-associated coiled-coil containing kinase1 (ROCK1) is associated with genetic instability and poor prognosis in prostate cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102294
                DO  - 10.18632/aging.102294
                SP  - 7859
                EP  - 7879
                PY  - 
                AB  - Background and objectives: Overexpression of the cytoskeleton-modulating kinase ROCK1 has been associated with unfavorable outcome in many cancers, but its impact in prostate cancer is largely unknown.Results: A weak ROCK1 staining was found in &gt;90% of normal, and cancerous prostate tissues, but was generally stronger in cancer cells as compared to adjacent normal glands. In cancer, ROCK1 staining was considered weak, moderate, and strong in 22%, 53%, and 18% of cases respectively. Higher ROCK1 expression levels were associated with tumor stage, and Gleason grade, positive nodal stage, positive surgical margin, accelerated cell proliferation and early PSA recurrence in multivariable analysis. ROCK1 up regulation was associated with androgen receptor (AR) expression, TMPRSS2:ERG fusion, genomic deletions of the PTEN tumor suppressor, as well as recurrent deletions at chromosomes 3p, 5q, 6q. Strong ROCK1 staining was found in 3% of AR-negative, but in 27% of strongly AR positive cancers, in 13% of ERG-negative but in 25% of ERG positive cancers, and in 12% of PTEN normal but in 26% of PTEN deleted cancers.Conclusions: This study identifies ROCK1 expression associated with prognosis in prostate cancer.Methods: We tested ROCK1 expression in 12 427 prostate cancer specimens and followed PSA recurrence after prostatectomy.
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Mechanisms of ROS-induced mitochondria-dependent apoptosis underlying liquid storage of goat spermatozoa

Tengfei Liu, Yawen Han, Ting Zhou, Ruihang Zhang, Hong Chen, Shulin Chen, Huiying Zhao,

https://doi.org/10.18632/aging.102295 pp 7880—7898

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Liu T, Han Y, Zhou T, Zhang R, Chen H, Chen S, Zhao H, . Mechanisms of ROS-induced mitochondria-dependent apoptosis underlying liquid storage of goat spermatozoa. . 11:7880-7898. https://doi.org/10.18632/aging.102295

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                TY  - JOUR
                AU  - Liu, Tengfei 
                AU  - Han, Yawen 
                AU  - Zhou, Ting 
                AU  - Zhang, Ruihang 
                AU  - Chen, Hong 
                AU  - Chen, Shulin 
                AU  - Zhao, Huiying 
                TI  - Mechanisms of ROS-induced mitochondria-dependent apoptosis underlying liquid storage of goat spermatozoa
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102295
                DO  - 10.18632/aging.102295
                SP  - 7880
                EP  - 7898
                PY  - 
                AB  - Liquid storage of spermatozoa is important for artificial insemination and herd genetic breeding. However, the extended time of storage inducing the rapid decline in spermatozoa quality limits the development of this technology. The molecular mechanisms underlying liquid storage of spermatozoa remain largely unexplored. In this study, the effects of liquid storage on functional quality of spermatozoa were assessed in goat (Capra hircus). The time-dependent decline in spermatozoa motility showed a strong correlation with the significant increase in apoptosis. Moreover, apoptosis-related ultrastructural changes were observed, especially the defects in mitochondria. A significant decrease in mitochondrial membrane potential and changes in the expression of mitochondrial apoptosis-related proteins indicated mitochondrial dysfunction and mitochondrial apoptotic pathway activation. Notably, the abnormally high level of reactive oxygen species (ROS) caused by liquid storage resulted in oxidative damage to mitochondria and accelerated mitochondria-dependent apoptosis, as demonstrated by the addition of ROS scavenger N-acetylcysteine. Furthermore, critical differentially expressed proteins involved in mitochondria-dependent apoptosis and antioxidant defense were identified and profiled by quantitative proteomic analysis, facilitating the understanding of molecular regulation of ROS-induced mitochondria-dependent apoptosis. These outcomes provide insights into the mechanisms underlying liquid storage of goat spermatozoa and enhance the progress of semen storage technology.
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Fibroblast growth factor 23 expression in human calcified vascular tissues

Javier Donate-Correa, Ernesto Martín-Núñez, Carolina Hernández-Carballo, Carla Ferri, Víctor G. Tagua, Alejandro Delgado-Molinos, Ángel López-Castillo, Sergio Rodríguez-Ramos, Purificación Cerro-López, Victoria Castro López-Tarruella, Raquel Felipe-García, Miguel A. Arévalo-Gomez, Nayra Pérez-Delgado, Carmen Mora-Fernández, Juan F. Navarro-González,

https://doi.org/10.18632/aging.102297 pp 7899—7913

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Donate-Correa J, Martín-Núñez E, Hernández-Carballo C, Ferri C, Tagua VG, Delgado-Molinos A, López-Castillo Á, Rodríguez-Ramos S, Cerro-López P, López-Tarruella VC, Felipe-García R, Arévalo-Gomez MA, Pérez-Delgado N, et al, . Fibroblast growth factor 23 expression in human calcified vascular tissues. . 11:7899-7913. https://doi.org/10.18632/aging.102297

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                TY  - JOUR
                AU  - Donate-Correa, Javier 
                AU  - Martín-Núñez, Ernesto 
                AU  - Hernández-Carballo, Carolina 
                AU  - Ferri, Carla 
                AU  - Tagua, Víctor G. 
                AU  - Delgado-Molinos, Alejandro 
                AU  - López-Castillo, Ángel 
                AU  - Rodríguez-Ramos, Sergio 
                AU  - Cerro-López, Purificación 
                AU  - López-Tarruella, Victoria Castro 
                AU  - Felipe-García, Raquel 
                AU  - Arévalo-Gomez, Miguel A. 
                AU  - Pérez-Delgado, Nayra 
                AU  - Mora-Fernández, Carmen 
                AU  - Navarro-González, Juan F. 
                TI  - Fibroblast growth factor 23 expression in human calcified vascular tissues
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102297
                DO  - 10.18632/aging.102297
                SP  - 7899
                EP  - 7913
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Donate-Correa, Javier 
                AU  - Martín-Núñez, Ernesto 
                AU  - Hernández-Carballo, Carolina 
                AU  - Ferri, Carla 
                AU  - Tagua, Víctor G. 
                AU  - Delgado-Molinos, Alejandro 
                AU  - López-Castillo, Ángel 
                AU  - Rodríguez-Ramos, Sergio 
                AU  - Cerro-López, Purificación 
                AU  - López-Tarruella, Victoria Castro 
                AU  - Felipe-García, Raquel 
                AU  - Arévalo-Gomez, Miguel A. 
                AU  - Pérez-Delgado, Nayra 
                AU  - Mora-Fernández, Carmen 
                AU  - Navarro-González, Juan F. 
                TI  - Fibroblast growth factor 23 expression in human calcified vascular tissues
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102297
                DO  - 10.18632/aging.102297
                SP  - 7899
                EP  - 7913
                PY  - 
                AB  - Vascular calcification is a major risk for cardiovascular disease and implies the transformation of smooth muscle cells to an osteoblastic phenotype as a consequence of dysregulation of calcium and phosphate metabolism. Fibroblast growth factor (FGF) 23 is the most potent phosphate regulator. Observational studies suggest that high levels of FGF23 are related to cardiovascular morbidity and mortality. In this work, we determined the levels of both the intact and the carboxi-terminal fragments of circulating FGF23 in 133 patients with established cardiovascular disease, the expression of FGF23, its receptors 1 and 3, and its co-receptor Klotho in vascular fragments of aorta, carotid and femoral in 43 out of this group of patients, and in a control group of 20 organ donors. Patients with atherosclerosis and vascular calcification presented increased levels of FGF23 respect to the control group. Vascular immunoreactivity for FGF23 was also significantly increased in patients with vascular calcification as compared to patients without calcification and to controls. Finally, gene expression of FGF23 and RUNX2 were also higher and directly related in vascular samples with calcification. Conversely, expression of Klotho was reduced in patients with cardiovascular disease when comparing to controls. In conclusion, our findings link the calcification of the vascular tissue with the expression of FGF23 in the vessels and with the elevation of circulating levels this hormone.
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TIP-B1 promotes kidney clear cell carcinoma growth and metastasis via EGFR/AKT signaling

Lei Yin, Shenglin Gao, Heng Shi, Keyi Wang, Huan Yang, Bo Peng,

https://doi.org/10.18632/aging.102298 pp 7914—7937

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Yin L, Gao S, Shi H, Wang K, Yang H, Peng B, . TIP-B1 promotes kidney clear cell carcinoma growth and metastasis via EGFR/AKT signaling. . 11:7914-7937. https://doi.org/10.18632/aging.102298

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                TY  - JOUR
                AU  - Yin, Lei 
                AU  - Gao, Shenglin 
                AU  - Shi, Heng 
                AU  - Wang, Keyi 
                AU  - Yang, Huan 
                AU  - Peng, Bo 
                TI  - TIP-B1 promotes kidney clear cell carcinoma growth and metastasis via EGFR/AKT signaling
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102298
                DO  - 10.18632/aging.102298
                SP  - 7914
                EP  - 7937
                PY  - 
                AB  - Kidney clear cell carcinoma (KIRC) is the most prevalent kidney malignancy. Accumulating evidence shows that high expression of TIP-B1 correlates with development of tumor progression. However, the detailed functions of TIP-B1 in the KIRC remain to be further elucidated. Here, we firstly found TIP-B1 expression was significantly increased in KIRC compared with adjacent normal tissues. What&#x2019;s more, higher expression of TIP-B1 were correlated with aggressive clinico-pathological characteristics. In vitro assay found TIP-B1 knockdown dramatically inhibited KIRC cells proliferation, migration and invasion. In vivo assay found down regulated TIP-B1 could suppress tumor growth and metastasis. Mechanism analysis indicated that TIP-B1 could bind EGFR and suppress EGFR degradation, then promoted EGF-induced AKT signaling. Together, TIP-B1 could be applied as an independent risk factor to predict KIRC progression and metastasis. Targeting TIP-B1 might be a new potential therapeutic strategy for KIRC treatment.
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The effects of dietary fatty acids on bone, hematopoietic marrow and marrow adipose tissue in a murine model of senile osteoporosis

Ebrahim Bani Hassan, Mostafa Alderghaffar, Fabien Wauquier, Veronique Coxam, Oddom Demontiero, Sara Vogrin, Yohann Wittrant, Gustavo Duque,

https://doi.org/10.18632/aging.102299 pp 7938—7947

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Bani Hassan E, Alderghaffar M, Wauquier F, Coxam V, Demontiero O, Vogrin S, Wittrant Y, Duque G, . The effects of dietary fatty acids on bone, hematopoietic marrow and marrow adipose tissue in a murine model of senile osteoporosis. . 11:7938-7947. https://doi.org/10.18632/aging.102299

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                TY  - JOUR
                AU  - Bani Hassan, Ebrahim 
                AU  - Alderghaffar, Mostafa 
                AU  - Wauquier, Fabien 
                AU  - Coxam, Veronique 
                AU  - Demontiero, Oddom 
                AU  - Vogrin, Sara 
                AU  - Wittrant, Yohann 
                AU  - Duque, Gustavo 
                TI  - The effects of dietary fatty acids on bone, hematopoietic marrow and marrow adipose tissue in a murine model of senile osteoporosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102299
                DO  - 10.18632/aging.102299
                SP  - 7938
                EP  - 7947
                PY  - 
                AB  - Purpose: Marrow adipose tissue (MAT) expansion and associated lipotoxicity are important drivers of age-related bone loss and hematopoietic bone marrow (HBM) atrophy. Fish oil and borage oil (rich in &#x3C9;3 fatty acids) can partially prevent aged-related bone loss in SAMP8 mice. However, whether preservation of bone mass in this progeria model is associated with MAT volumes remains unknown.Results: MAT volume fraction (MAT%) showed a negative association with hematopoietic bone marrow (HBM%;r=-0.836, p&lt;0.001) and bone (bone%;r=-0.344, p=0.013) volume fractions.Adjusting for multiple comparisons, bone% was higher and MAT% was lower in Fish oil (FO)-supplemented groups vs. controls (p&lt;0.001). HBM% did not differ significantly between the four groups. However, in the group supplemented with FO, HBM comprised higher fractions and MAT constituted lower fractions of total marrow vs. controls (p&lt;0.001).Conclusion: Feeding FO-enriched diet prevented age-related bone and HBM loss, by reducing MAT expansion. Our results further emphasize on the role(s) of MAT expansion in bone and HBM atrophy.Methods: SAMP8 mice (n&gt;9 /group) were allocated into 4 categories and fed a control ration, FO-, sunflower oil (SFO)- and borage oil-enriched diets for lifetime. Femurs were scanned using microcomputed tomography (&#x3BC;CT) and bone, MAT, and HBM volumes were determined using an image analysis software.
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Prevalence and prognosis significance of cardiovascular disease in cancer patients: a population-based study

Dong Liu, Zhiqiang Ma, Jingang Yang, Min Zhao, Huiping Ao, Xiaodong Zheng, Qianfa Wen, Yuejin Yang, Jiangyun You, Shubin Qiao, Jiansong Yuan,

https://doi.org/10.18632/aging.102301 pp 7948—7960

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Liu D, Ma Z, Yang J, Zhao M, Ao H, Zheng X, Wen Q, Yang Y, You J, Qiao S, Yuan J, . Prevalence and prognosis significance of cardiovascular disease in cancer patients: a population-based study. . 11:7948-7960. https://doi.org/10.18632/aging.102301

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                TY  - JOUR
                AU  - Liu, Dong 
                AU  - Ma, Zhiqiang 
                AU  - Yang, Jingang 
                AU  - Zhao, Min 
                AU  - Ao, Huiping 
                AU  - Zheng, Xiaodong 
                AU  - Wen, Qianfa 
                AU  - Yang, Yuejin 
                AU  - You, Jiangyun 
                AU  - Qiao, Shubin 
                AU  - Yuan, Jiansong 
                TI  - Prevalence and prognosis significance of cardiovascular disease in cancer patients: a population-based study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102301
                DO  - 10.18632/aging.102301
                SP  - 7948
                EP  - 7960
                PY  - 
                AB  - Background: Cardiovascular disease (CVD) is a heavy burden on cancer patients worldwide. This study aimed to evaluate the prevalence and influence of cardiovascular risk factors (CVRF) and CVD on the all-cause mortality among Chinese cancer patients.Results: Overall, 13.0% of all cancer patients had at least one type of CVRFs and 5.0% with CVDs. Patients with CVRF or CVD presented more frequently at later stages and received higher percentage of oncotherapy. During 1,782,527 person-years of follow-up, the all-cause mortality in cancer patients with CVDs and with CVRFs was higher compared with those without (182.6/1000, 109.5/1000 and 93.3/1000 person-years, respectively). Cox regression analysis showed that patients with heart failure (HR 1.79, 95% CI 1.61-1.99), myocardial infarction (HR 1.50, 95% CI 1.16-1.95), atrial fibrillation (HR 1.30, 95% CI 1.09-1.53), stroke (HR 1.21, 95% CI 1.11-1.32), hypertension (HR 1.10, 95% CI 1.04-1.16) and diabetes (HR 1.16, 95% CI 1.08-1.24) had increased all-cause mortality, whereas dyslipidemia patients had better prognosis (HR 0.73, 95% CI 0.64-0.83). Stratified by cancer type, the prognostic impact of specific CVRF or CVD varied.Methods: We consecutively recruited 710,170 cancer patients between Feb. 1995 and Jun. 2018. A stratified Cox proportional hazards model was used to analyze the effect of comorbidities on the overall survival of patients stratified by cancer type.Conclusions: Cancer patients are vulnerable to comorbidity related to heart and cerebral disease. The influence of comorbidities on prognosis is noticeable and specific both for the type of cancer and comorbidities.
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Kinsenoside ameliorates intervertebral disc degeneration through the activation of AKT-ERK1/2-Nrf2 signaling pathway

Yanqiu Wang, Rui Zuo, Ziwen Wang, Liwen Luo, Junlong Wu, Chao Zhang, Minghan Liu, Chunmeng Shi, Yue Zhou,

https://doi.org/10.18632/aging.102302 pp 7961—7977

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Wang Y, Zuo R, Wang Z, Luo L, Wu J, Zhang C, Liu M, Shi C, Zhou Y, . Kinsenoside ameliorates intervertebral disc degeneration through the activation of AKT-ERK1/2-Nrf2 signaling pathway. . 11:7961-7977. https://doi.org/10.18632/aging.102302

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                TY  - JOUR
                AU  - Wang, Yanqiu 
                AU  - Zuo, Rui 
                AU  - Wang, Ziwen 
                AU  - Luo, Liwen 
                AU  - Wu, Junlong 
                AU  - Zhang, Chao 
                AU  - Liu, Minghan 
                AU  - Shi, Chunmeng 
                AU  - Zhou, Yue 
                TI  - Kinsenoside ameliorates intervertebral disc degeneration through the activation of AKT-ERK1/2-Nrf2 signaling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102302
                DO  - 10.18632/aging.102302
                SP  - 7961
                EP  - 7977
                PY  - 
                AB  - Intervertebral disc degeneration (IDD) is recognized as the major contributor to low back pain, which results in disability worldwide and heavy burdens on society and economy. Here we present evidence that the lower level of Nrf2 is closely associated with higher grade of IDD. The apoptosis and senescence of nucleus pulposus cells (NPCs) were exacerbated by Nrf2 knockdown, but suppressed by Nrf2 overexpression under oxidative stress. Based on findings that Kinsenoside could exert multiple pharmacological effects, we found that Kinsenoside rescued the NPC viability under oxidative stress and protected against apoptosis, senescence and mitochondrial dysfunction in a Nrf2-dependent way. Further experiments revealed that Kinsenoside activated a signaling pathway of AKT-ERK1/2-Nrf2 in NPCs. Moreover, in vivo study showed that Kinsenoside ameliorated IDD in a puncture-induced model. Together, the present work suggests that Nrf2 is involved in the pathogenesis of IDD and shows the protective effects as well as the underlying mechanism of Kinsenoside on Nrf2 activation in NPCs.
                ER  -

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GSK-3β and ERK1/2 incongruously act in tau hyperphosphorylation in SPS-induced PTSD rats

Zhen Wei, Yacoubou Abdoul Razak Mahaman, Feiqi Zhu, Mengjuan Wu, Yiyuan Xia, Kuan Zeng, Ying Yang, Rong Liu, Jian-Zhi Wang, Xiji Shu, Xiaochuan Wang,

https://doi.org/10.18632/aging.102303 pp 7978—7995

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Wei Z, Mahaman YAR, Zhu F, Wu M, Xia Y, Zeng K, Yang Y, Liu R, Wang J, Shu X, Wang X, . GSK-3β and ERK1/2 incongruously act in tau hyperphosphorylation in SPS-induced PTSD rats. . 11:7978-7995. https://doi.org/10.18632/aging.102303

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                TY  - JOUR
                AU  - Wei, Zhen 
                AU  - Mahaman, Yacoubou Abdoul Razak 
                AU  - Zhu, Feiqi 
                AU  - Wu, Mengjuan 
                AU  - Xia, Yiyuan 
                AU  - Zeng, Kuan 
                AU  - Yang, Ying 
                AU  - Liu, Rong 
                AU  - Wang, Jian-Zhi 
                AU  - Shu, Xiji 
                AU  - Wang, Xiaochuan 
                TI  - GSK-3β and ERK1/2 incongruously act in tau hyperphosphorylation in SPS-induced PTSD rats
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102303
                DO  - 10.18632/aging.102303
                SP  - 7978
                EP  - 7995
                PY  - 
                AB  - Post-traumatic stress disorder (PTSD) manifests in neurocognitive deficits in association with increased tau deposition, which mainly consist of phosphorylated tau in Alzheimer disease (AD) brain. However, the exact mechanism of PTSD inducing tau hyperphosphorylation remains unclear and therefore no effective treatment options are currently available. We here show that employing single prolonged stress (SPS), as a consensus PTSD model, induced a typical anxiety and abnormal hyperphosphorylation of tau at Ser202/Thr205 (AT8) and Ser404 but not at Ser199 and Ser396 in the hippocampus compared to the control rats. Furthermore, there was a decrease in the level of inactivated phosphorylated GSK-3&#x3B2; at Ser9, an increase in the level of activated phosphorylated GSK-3&#x3B2; at Thr216 and an obvious decrease in the level of activated phosphorylated ERK1/2, but no alterations in CaMKII and PP2A in hippocampus of SPS rats. On the other hand, the levels of both phosphorylated AKT and total SGK1, stress- and GSK-3&#x3B2;/ERK1/2-related proteins, were down-regulated. Interestingly, Overexpression of SGK1 increased the level of phosphorylated ERK1/2 and led to tau hyperphosphorylation at Ser199 and Ser396. These findings suggest that SPS exposure results in differential tau phosphorylation at different sites probably due to incongruous action between AKT-related GSK-3&#x3B2; activation and SGK1-related ERK1/2 inactivation, suggesting a link between SPS-induced PTSD and AD-associated tau pathogenic mechanisms.
                ER  -

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Differential effects of extracellular vesicles from aging and young mesenchymal stem cells in acute lung injury

Ruoqiong Huang, Chaojin Qin, Jiangmei Wang, Yaoqin Hu, Guoping Zheng, Guanguan Qiu, Menghua Ge, Huikang Tao, Qiang Shu, Jianguo Xu,

https://doi.org/10.18632/aging.102314 pp 7996—8014

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Huang R, Qin C, Wang J, Hu Y, Zheng G, Qiu G, Ge M, Tao H, Shu Q, Xu J, . Differential effects of extracellular vesicles from aging and young mesenchymal stem cells in acute lung injury. . 11:7996-8014. https://doi.org/10.18632/aging.102314

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                TY  - JOUR
                AU  - Huang, Ruoqiong 
                AU  - Qin, Chaojin 
                AU  - Wang, Jiangmei 
                AU  - Hu, Yaoqin 
                AU  - Zheng, Guoping 
                AU  - Qiu, Guanguan 
                AU  - Ge, Menghua 
                AU  - Tao, Huikang 
                AU  - Shu, Qiang 
                AU  - Xu, Jianguo 
                TI  - Differential effects of extracellular vesicles from aging and young mesenchymal stem cells in acute lung injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102314
                DO  - 10.18632/aging.102314
                SP  - 7996
                EP  - 8014
                PY  - 
                AB  - Old age is a known risk factor for mortality in acute respiratory distress syndrome (ARDS)/acute lung injury. Mesenchymal stem cells (MSCs) possess potent immunomodulatory properties, while aging MSCs have reduced capacity. Recent studies have demonstrated that MSC-derived extracellular vesicles (MSC-EVs) are able to mimic MSCs in alleviating acute lung injury. The goals of this study were to determine whether EVs from young and aging MSCs had differential effects on lipopolysaccharide (LPS)-induced lung injury in young mice and unravel the underlying mechanisms. Our results showed that both aging and young MSC-EVs had similar physical and phenotypical properties. As their parental cells, young MSC-EVs alleviated LPS-induced acute lung injury, while aging MSC-EVs did not exhibit the protective effects. In contrast to young MSC-EVs, aging MSC-EVs failed to alter macrophage phenotypes and reduce macrophage recruitment. In addition, the internalization of aging MSC-EVs by macrophages was significantly lower compared with that of young MSC-EVs. Furthermore, aging and young MSC-EVs differed in levels of several miRNAs relating macrophage polarization. In conclusion, aging and young MSC-EVs have differential effects in alleviating acute lung injury and macrophage polarization, which may be associated with internalization of EVs and their miRNA content.
                ER  -

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Circular RNA profiling in the oocyte and cumulus cells reveals that circARMC4 is essential for porcine oocyte maturation

Zubing Cao, Di Gao, Tengteng Xu, Ling Zhang, Xu Tong, Dandan Zhang, Yiqing Wang, Wei Ning, Xin Qi, Yangyang Ma, Kaiyuan Ji, Tong Yu, Yunsheng Li, Yunhai Zhang,

https://doi.org/10.18632/aging.102315 pp 8015—8034

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Cao Z, Gao D, Xu T, Zhang L, Tong X, Zhang D, Wang Y, Ning W, Qi X, Ma Y, Ji K, Yu T, Li Y, et al, . Circular RNA profiling in the oocyte and cumulus cells reveals that circARMC4 is essential for porcine oocyte maturation. . 11:8015-8034. https://doi.org/10.18632/aging.102315

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                TY  - JOUR
                AU  - Cao, Zubing 
                AU  - Gao, Di 
                AU  - Xu, Tengteng 
                AU  - Zhang, Ling 
                AU  - Tong, Xu 
                AU  - Zhang, Dandan 
                AU  - Wang, Yiqing 
                AU  - Ning, Wei 
                AU  - Qi, Xin 
                AU  - Ma, Yangyang 
                AU  - Ji, Kaiyuan 
                AU  - Yu, Tong 
                AU  - Li, Yunsheng 
                AU  - Zhang, Yunhai 
                TI  - Circular RNA profiling in the oocyte and cumulus cells reveals that circARMC4 is essential for porcine oocyte maturation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102315
                DO  - 10.18632/aging.102315
                SP  - 8015
                EP  - 8034
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cao, Zubing 
                AU  - Gao, Di 
                AU  - Xu, Tengteng 
                AU  - Zhang, Ling 
                AU  - Tong, Xu 
                AU  - Zhang, Dandan 
                AU  - Wang, Yiqing 
                AU  - Ning, Wei 
                AU  - Qi, Xin 
                AU  - Ma, Yangyang 
                AU  - Ji, Kaiyuan 
                AU  - Yu, Tong 
                AU  - Li, Yunsheng 
                AU  - Zhang, Yunhai 
                TI  - Circular RNA profiling in the oocyte and cumulus cells reveals that circARMC4 is essential for porcine oocyte maturation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102315
                DO  - 10.18632/aging.102315
                SP  - 8015
                EP  - 8034
                PY  - 
                AB  - Thousands of circular RNAs (circRNAs) have been recently discovered in cumulus cells and oocytes from several species. However, the expression and function of circRNA during porcine oocyte meiotic maturation have been never examined. Here, we separately identified 7,067 and 637 circRNAs in both cumulus cells and oocytes via deep sequencing and bioinformatic analysis. Further analysis revealed that a faction of circRNAs is differentially expressed (DE) in a developmental stage-specific manner. The host genes of DE circRNAs are markedly enriched to multiple signaling pathways associated with cumulus cell function and oocyte maturation. Additionally, most DE circRNAs harbor several miRNA targets, suggesting that these DE circRNAs potentially act as miRNA sponge. Importantly, we found that maternal circARMC4 knockdown by siRNA microinjection caused a severely impaired chromosome alignment, and significantly inhibited first polar body extrusion and early embryo development. Taken together, these results demonstrate for the first time that circRNAs are abundantly and dynamically expressed in a developmental stage-specific manner in cumulus cells and oocytes, and maternally expressed circARMC4 is essential for porcine oocyte meiotic maturation and early embryo development.
                ER  -

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Correction for: Aged cells in human skeletal muscle after resistance exercise

Chi Yang, Ying Jiao, Bing Wei, Zeyi Yang, Jin-Fu Wu, Jorgen Jensen, Wei-Horng Jean, Chih-Yang Huang, Chia-Hua Kuo,

https://doi.org/10.18632/aging.102338 pp 8035

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Yang C, Jiao Y, Wei B, Yang Z, Wu J, Jensen J, Jean W, Huang C, Kuo C, . Correction for: Aged cells in human skeletal muscle after resistance exercise. . 11:8035-8035. https://doi.org/10.18632/aging.102338

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Volume 11, Issue 18

About the Cover

Editorials

Raymond Noordam, William J. Young, Patricia B. Munroe,

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Sara Ancel, Omid Mashinchian, Jerome N. Feige,

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Xingzhe Ma, Qing Yi,

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Boyan K. Garvalov, Sajjad Muhammad, Gergana Dobreva,

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Research Papers

Peng Chen, Fuchao Chen, Ben-hong Zhou,

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Xueni Xu, Xiaoxiang Chen, Mu Xu, Xiangxiang Liu, Bei Pan, Jian Qin, Tao Xu, Kaixuan Zeng, Yuqin Pan, Bangshun He, Huiling Sun, Li Sun, Shukui Wang,

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Yongchun Zhou, Hutao Shi, Yaqian Du, Guangqiang Zhao, Xiaoxiong Wang, Quan Li, Junxi Liu, Lianhua Ye, Zhenghai Shen, Yinjin Guo, Yunchao Huang,

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Pengfei Wang, Xiangbei Qi, Guohui Xu, Jianning Liu, Jichao Guo, Xu Li, Xinzhe Ma, Hui Sun,

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Xin Lin, Gen Li, Yu Zhang, Jingjing Zhao, Jiawen Lu, Yunge Gao, Huihui Liu, Geng-Lin Li, Tao Yang, Lei Song, Hao Wu,

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Xuan Jing, Hongping Liang, Chonghua Hao, Li Hongxia, Xiangrong Cui,

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Yong Hao, Jie Ding, Ronghua Hong, Shuwei Bai, Ze Wang, Chengjun Mo, Qiang Hu, Zezhi Li, Yangtai Guan,

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Er-Bao Chen, Xuan Qin, Ke Peng, Qian Li, Cheng Tang, Yi-Chou Wei, Shan Yu, Lu Gan, Tian-Shu Liu,

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Ting Qiu, Yaqiong Tian, Yujuan Gao, Miao Ma, Hui Li, Xiaoqin Liu, Hongyan Wu, Yingwei Zhang, Hui Ding, Mengshu Cao, Ji Zhang, Jinghong Dai, Jingyu Chen, Hourong Cai,

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Tianbao Chen, Yi Zhang, Yilan Liu, Dexiao Zhu, Jing Yu, Guoqian Li, Zhichun Sun, Wanru Wang, Hongwei Jiang, Zhenzhen Hong,

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Jianguo Lai, Bo Chen, Guochun Zhang, Yulei Wang, Hsiaopei Mok, Lingzhu Wen, Zihao Pan, Fengxi Su, Ning Liao,

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Jun Ma, Changgui Shi, Zhongyang Liu, Bin Han, Lei Guo, Lei Zhu, Tianwen Ye,

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Shenghu Guo, Lei Zhang, Yuehua Zhang, Zheng Wu, Dongwei He, Xing Li, Zhiyu Wang,

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Qian Su, Peng Zhang, Dong Yu, Zhaodi Wu, Dandan Li, Fangfang Shen, Pengfei Liao, Guizhi Yin,

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Corey R. Hart, Zachary C. Ryan, Kyle T. Pfaffenbach, Surendra Dasari, Mojtaba Parvizi, Antigoni Z. Lalia, Ian R. Lanza,

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