Volume 11, Issue 20

Ge X, Xu B, Xu W, Xia L, Xu Z, Shen L, Peng W, Huang S, . Long noncoding RNA GAS5 inhibits cell proliferation and fibrosis in diabetic nephropathy by sponging miR-221 and modulating SIRT1 expression. . 11:8745-8759. https://doi.org/10.18632/aging.102249

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                TY  - JOUR
                AU  - Ge, Xiaoxu 
                AU  - Xu, Bojin 
                AU  - Xu, Wenwei 
                AU  - Xia, Lili 
                AU  - Xu, Zhongqin 
                AU  - Shen, Lisha 
                AU  - Peng, Wenfang 
                AU  - Huang, Shan 
                TI  - Long noncoding RNA GAS5 inhibits cell proliferation and fibrosis in diabetic nephropathy by sponging miR-221 and modulating SIRT1 expression
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102249
                DO  - 10.18632/aging.102249
                SP  - 8745
                EP  - 8759
                PY  - 
                AB  - Diabetic nephropathy (DN) is one of the leading causes of end-stage renal diseases worldwide. This study is designed to investigate the underlying function and mechanism of a novel lncRNA GAS5 in the progression of DN. We found that lncRNA GAS5 expression level was decreased in type 2 diabetes (T2D) with DN compared with that in patients without DN. Moreover, lncRNA GAS5 expression level was negatively associated with the severity of DN-related complications. lncRNA GAS5 inhibited MCs proliferation and caused G0/1 phase arrest. lncRNA GAS5 overexpression alleviated the expression of fibrosis-related protein in mesangial cells (MCs). The dual-luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay results revealed that lncRNA GAS5 functions as an endogenous sponge for miR-221 via both the directly targeting way and Ago2-dependent manner. Furthermore, SIRT1 was confirmed as a target gene of miR-221. lncRNA GAS5 upregulated SIRT1 expression and inhibited MCs proliferation and fibrosis by acting as an miR-221 sponge. Finally, we found that lncRNA GSA5 suppressed the development of DN in vivo. Thus, lncRNA GAS5 was involved in the progression of DN by sponging miR-221 and contributed to lncRNA-directed diagnostics and therapeutics in DN.
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Adipose tissue-derived omentin-1 attenuates arterial calcification via AMPK/Akt signaling pathway

Feng Xu, Fu-Xing-Zi Li, Xiao Lin, Jia-Yu Zhong, Feng Wu, Su-Kang Shan, Chang-Ming Tan, Ling-Qing Yuan, Xiao-Bo Liao,

https://doi.org/10.18632/aging.102251 pp 8760—8776

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Xu F, Li F, Lin X, Zhong J, Wu F, Shan S, Tan C, Yuan L, Liao X, . Adipose tissue-derived omentin-1 attenuates arterial calcification via AMPK/Akt signaling pathway. . 11:8760-8776. https://doi.org/10.18632/aging.102251

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                TY  - JOUR
                AU  - Xu, Feng 
                AU  - Li, Fu-Xing-Zi 
                AU  - Lin, Xiao 
                AU  - Zhong, Jia-Yu 
                AU  - Wu, Feng 
                AU  - Shan, Su-Kang 
                AU  - Tan, Chang-Ming 
                AU  - Yuan, Ling-Qing 
                AU  - Liao, Xiao-Bo 
                TI  - Adipose tissue-derived omentin-1 attenuates arterial calcification via AMPK/Akt signaling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102251
                DO  - 10.18632/aging.102251
                SP  - 8760
                EP  - 8776
                PY  - 
                AB  - Adipose tissue-derived adipokines mediate various kind of crosstalk between adipose tissue and other organs and thus regulate metabolism balance, inflammation state as well as disease progression. In particular, omentin-1, a newly found adipokine, has been reported to exhibit anti-calcification effects in vitro and in vivo. However, little is known about the function of endogenous adipose tissue-derived omentin-1 in arterial calcification and the detailed mechanism involved. Here, we demonstrated that global omentin-1 knockout (omentin-1-/-) resulted in more obvious arterial calcification in 5/6-nephrectomy plus high phosphate diet treated (5/6 NTP) mice while overexpression of omentin-1 attenuated attenuates osteoblastic differentiation and mineralisation of VSMCs in vitro and 5/6 NTP-induced mice arterial calcification in vivo. Moreover, we found that omentin-1 induced AMPK and Akt activation while inhibition of AMP-activated protein kinase (AMPK) and Akt signaling reversed the anti-calcification effect induced by omentin-1 both in vitro and in vivo. Our results suggest that adipose tissue-derived omentin-1 serves as a potential therapeutic target for arterial calcification and cardiovascular disease.
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LncRNA MALAT1 shuttled by bone marrow-derived mesenchymal stem cells-secreted exosomes alleviates osteoporosis through mediating microRNA-34c/SATB2 axis

Xucheng Yang, Junxiao Yang, Pengfei Lei, Ting Wen,

https://doi.org/10.18632/aging.102264 pp 8777—8791

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Yang X, Yang J, Lei P, Wen T, . LncRNA MALAT1 shuttled by bone marrow-derived mesenchymal stem cells-secreted exosomes alleviates osteoporosis through mediating microRNA-34c/SATB2 axis. . 11:8777-8791. https://doi.org/10.18632/aging.102264

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                TY  - JOUR
                AU  - Yang, Xucheng 
                AU  - Yang, Junxiao 
                AU  - Lei, Pengfei 
                AU  - Wen, Ting 
                TI  - LncRNA MALAT1 shuttled by bone marrow-derived mesenchymal stem cells-secreted exosomes alleviates osteoporosis through mediating microRNA-34c/SATB2 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102264
                DO  - 10.18632/aging.102264
                SP  - 8777
                EP  - 8791
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) have emerged as promising novel modulators during osteogenesis in mesenchymal stem cells (MSCs). Enhanced SATB2 has been demonstrated to promote osteogenic differentiation of bone marrow-derived mesenchymal stem cells (hBMSCs) in patients with osteonecrosis. Preliminary bioinformatic analysis identified putative binding sites between microRNA-34c (miR-34c) and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) or miR-34c and SATB2 3&#x2019;UTR. Thus, the current study aimed to clarify the potential functional relevance of MALAT1-containing exosomes from BMSCs in osteoporosis. The extracted exosomes from primary BMSCs were co-cultured with human osteoblasts (hFOB1.19), followed by evaluation of the hFOB1.19 cell proliferation, alkaline phosphatase (ALP) activity and mineralized nodules. The obtained findings indicated that BMSC-Exos promoted the expression of SATB2 in osteoblasts, and SATB2 silencing reduced the ALP activity of osteoblasts and mineralized nodules. MALAT1 acted as a sponge of miR-34c to promote the expression of SATB2. Additionally, BMSCs-derived exosomal MALAT1 promoted osteoblast activity. Moreover, in vivo experiments indicated that miR-34c reversed the effect of MALAT1, and SATB2 reversed the effect of miR-34c in ovariectomized mice. Taken together, this study demonstrates that BMSCs-derived exosomal MALAT1 enhances osteoblast activity in osteoporotic mice by mediating the miR-34c/SATB2 axis.
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Long non-coding RNA MALAT1 promotes cardiac remodeling in hypertensive rats by inhibiting the transcription of MyoD

Dan Li, Chunling Zhang, Jian Li, Jinna Che, Xuecheng Yang, Yuxin Xian, Xueli Li, Caixia Cao,

https://doi.org/10.18632/aging.102265 pp 8792—8809

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Li D, Zhang C, Li J, Che J, Yang X, Xian Y, Li X, Cao C, . Long non-coding RNA MALAT1 promotes cardiac remodeling in hypertensive rats by inhibiting the transcription of MyoD. . 11:8792-8809. https://doi.org/10.18632/aging.102265

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                TY  - JOUR
                AU  - Li, Dan 
                AU  - Zhang, Chunling 
                AU  - Li, Jian 
                AU  - Che, Jinna 
                AU  - Yang, Xuecheng 
                AU  - Xian, Yuxin 
                AU  - Li, Xueli 
                AU  - Cao, Caixia 
                TI  - Long non-coding RNA MALAT1 promotes cardiac remodeling in hypertensive rats by inhibiting the transcription of MyoD
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102265
                DO  - 10.18632/aging.102265
                SP  - 8792
                EP  - 8809
                PY  - 
                AB  - Hypertension is the leading preventable cause of premature deaths worldwide. Although long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been identified to play important roles in the development of cardiovascular diseases, the regulatory function of lncRNA MALAT1 in hypertension remains poorly understood. This study aimed to explore the role of lncRNA MALAT1 in spontaneously hypertensive rats (SHRs). LncRNA MALAT1 was determined to be elevated and MyoD to be reduced in myocardial tissues and thoracic aortic vascular tissues of SHRs. Over-expression of lncRNA MALAT1 caused severe myocardial fibrosis in SHRs. In addition, lncRNA MALAT1 over-expression in vitro enhanced arterial smooth muscle cells (ASMCs) activity and fibrosis of SHRs, which, was rescued by over-expressed MyoD. Furthermore, lncRNA MALAT1 transcripts were found to be highly enriched in the nucleus, and lncRNA MALAT1 suppressed the transactivation of MyoD. Moreover, lncRNA MALAT1 was found to recruit Suv39h1 to MyoD-binding loci, leading to H3K9me3 trimethylation and down-regulation of the target gene. Taken conjointly, this study revealed an important role of lncRNA MALAT1 in promoting cardiac remodeling in hypertensive rats by inhibiting the transcription of MyoD. These results highlight the value of lncRNA MALAT1 as a therapeutic target for the management of hypertension.
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Increased calcium channel in the lamina propria of aging rat

Ji Min Kim, Hyoung-Sam Heo, Sung-Chan Shin, Hyun-Keun Kwon, Jin-Choon Lee, Eui-Suk Sung, Hyung-Sik Kim, Gi Cheol Park, Byung-Joo Lee,

https://doi.org/10.18632/aging.102284 pp 8810—8824

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Kim JM, Heo H, Shin S, Kwon H, Lee J, Sung E, Kim H, Park GC, Lee B, . Increased calcium channel in the lamina propria of aging rat. . 11:8810-8824. https://doi.org/10.18632/aging.102284

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                TY  - JOUR
                AU  - Kim, Ji Min 
                AU  - Heo, Hyoung-Sam 
                AU  - Shin, Sung-Chan 
                AU  - Kwon, Hyun-Keun 
                AU  - Lee, Jin-Choon 
                AU  - Sung, Eui-Suk 
                AU  - Kim, Hyung-Sik 
                AU  - Park, Gi Cheol 
                AU  - Lee, Byung-Joo 
                TI  - Increased calcium channel in the lamina propria of aging rat
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102284
                DO  - 10.18632/aging.102284
                SP  - 8810
                EP  - 8824
                PY  - 
                AB  - The alterations of the extracellular matrix (ECM) in lamina propria of the vocal folds are important changes that are associated with decreased vibrations and increased stiffness in aging vocal fold. The aim of this study was to investigate the differences in gene expression of lamina propria using next generation sequencing (NGS) in young and aging rats and to identify genes that affect aging-related ECM changes for developing novel therapeutic target molecule. Among the 40 genes suggested in the NGS analysis, voltage-gated calcium channels (VGCC) subunit alpha1 S (CACNA1S), VGCC auxiliary subunit beta 1 (CACNB1), and VGCC auxiliary subunit gamma 1 (CACNG1) were increased in the lamina propria of the old rats compared to the young rats. The synthesis of collagen I and III in hVFFs decreased after si-CACNA1S and verapamil treatment. The expression and activity of matrix metalloproteinases (MMP)-1 and -8 were increased in hVFFs after the treatment of verapamil. However, there was no change in the expression of MMP-2 and -9. These results suggest that some calcium channels may be related with the alteration of aging-related ECM in vocal folds. Calcium channel has promising potential as a novel therapeutic target for the remodeling ECM of aging lamina propria.
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ACADS acts as a potential methylation biomarker associated with the proliferation and metastasis of hepatocellular carcinomas

Diyu Chen, Xiaode Feng, Zhen Lv, Xiaofeng Xu, Yuejie Lu, Wenxuan Wu, Hao Wu, Hua Liu, Linping Cao, Sunyi Ye, Jianzhong Chen, Jian Wu,

https://doi.org/10.18632/aging.102292 pp 8825—8844

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Chen D, Feng X, Lv Z, Xu X, Lu Y, Wu W, Wu H, Liu H, Cao L, Ye S, Chen J, Wu J, . ACADS acts as a potential methylation biomarker associated with the proliferation and metastasis of hepatocellular carcinomas. . 11:8825-8844. https://doi.org/10.18632/aging.102292

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                TY  - JOUR
                AU  - Chen, Diyu 
                AU  - Feng, Xiaode 
                AU  - Lv, Zhen 
                AU  - Xu, Xiaofeng 
                AU  - Lu, Yuejie 
                AU  - Wu, Wenxuan 
                AU  - Wu, Hao 
                AU  - Liu, Hua 
                AU  - Cao, Linping 
                AU  - Ye, Sunyi 
                AU  - Chen, Jianzhong 
                AU  - Wu, Jian 
                TI  - ACADS acts as a potential methylation biomarker associated with the proliferation and metastasis of hepatocellular carcinomas
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102292
                DO  - 10.18632/aging.102292
                SP  - 8825
                EP  - 8844
                PY  - 
                AB  - Background: Hepatocellular carcinomas (HCC) constantly rank among the malignancies with the highest death tolls on the global scale. Moreover, HCC are associated with a limited set of therapeutic options. This is particularly true in the case of advanced stage cancers, where long-term survival is uncommon. For the inoperable, advanced HCC patients, chemotherapy is the main modality of treatment. Due to the lack of known molecular targets, the efficacy of the chemotherapy is limited.Conclusion: These findings clearly indicate that DNA methylation plays a key role in regulating ACADS expression and that it can be a potential therapeutic target for treating HCC.Materials and methods: A thorough comparative analysis of 282 cancer samples with 47 normal samples from GEO datasets resulted in the observation that that the level of ACADS was significantly downregulated in HCC. Loss-of-function analyses were then conducted to understand the biological function of ACADS in HCC. It was noted that ACADS was involved in the proliferation and metastasis of HCC. Experiments involving the knockdown of DMNT expression led to the discovery that the expression of ACADS in the HCC cells was significantly increased. The TCGA database was then employed to identify tumor tissue samples which showed higher methylation levels at cg01535453, cg08618068, and cg10174836 (which are the target sites of the ACADS CpG islands) as compared with normal liver tissue samples. All these findings indicated that ACADS might be a novel methylation biomarker associated with HCC.
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COL6A6 interacted with P4HA3 to suppress the growth and metastasis of pituitary adenoma via blocking PI3K-Akt pathway

Ruiqing Long, Zhuohui Liu, Jinghui Li, Hualin Yu,

https://doi.org/10.18632/aging.102300 pp 8845—8859

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Long R, Liu Z, Li J, Yu H, . COL6A6 interacted with P4HA3 to suppress the growth and metastasis of pituitary adenoma via blocking PI3K-Akt pathway. . 11:8845-8859. https://doi.org/10.18632/aging.102300

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                TY  - JOUR
                AU  - Long, Ruiqing 
                AU  - Liu, Zhuohui 
                AU  - Li, Jinghui 
                AU  - Yu, Hualin 
                TI  - COL6A6 interacted with P4HA3 to suppress the growth and metastasis of pituitary adenoma via blocking PI3K-Akt pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102300
                DO  - 10.18632/aging.102300
                SP  - 8845
                EP  - 8859
                PY  - 
                AB  - The role and mechanism of collagen type VI alpha 6 (COL6A6) on tumor growth and metastasis in pituitary adenoma (PA) was determined. COL6A6 was downregulated in PA tissues and cell lines, which was negatively associated with the expression of prolyl-4-hydroxylase alpha polypeptide III (P4HA3) in the progression of PA. Overexpression of COL6A6 significantly suppressed tumor growth and metastasis capacity in PA. In addition, P4HA3 worked as the upstream of the PI3K-Akt pathway to alleviate the antitumor activity of COL6A6 on the growth and metastasis of both AtT-20 and HP75 cells. Furthermore, the inhibitory effect of COL6A6 on cell proliferation, migration and invasion, and epithelial-mesenchymal transition (EMT) was reversed by P4HA3 overexpression or activation of the PI3K-Akt pathway induced by IGF-1 addition, which provided a new biomarker for clinical PA treatment.
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Long non-coding SBF2-AS1 acting as a competing endogenous RNA to sponge microRNA-142-3p to participate in gemcitabine resistance in pancreatic cancer via upregulating TWF1

Yong-Qiang Hua, Yao-Dong Zhu, Guo-Qun Xie, Ke Zhang, Jie Sheng, Zhen-Feng Zhu, Zhou-Yu Ning, Hao Chen, Zhen Chen, Zhi-Qiang Meng, Lu-Ming Liu,

https://doi.org/10.18632/aging.102307 pp 8860—8878

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Hua Y, Zhu Y, Xie G, Zhang K, Sheng J, Zhu Z, Ning Z, Chen H, Chen Z, Meng Z, Liu L, . Long non-coding SBF2-AS1 acting as a competing endogenous RNA to sponge microRNA-142-3p to participate in gemcitabine resistance in pancreatic cancer via upregulating TWF1. . 11:8860-8878. https://doi.org/10.18632/aging.102307

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                TY  - JOUR
                AU  - Hua, Yong-Qiang 
                AU  - Zhu, Yao-Dong 
                AU  - Xie, Guo-Qun 
                AU  - Zhang, Ke 
                AU  - Sheng, Jie 
                AU  - Zhu, Zhen-Feng 
                AU  - Ning, Zhou-Yu 
                AU  - Chen, Hao 
                AU  - Chen, Zhen 
                AU  - Meng, Zhi-Qiang 
                AU  - Liu, Lu-Ming 
                TI  - Long non-coding SBF2-AS1 acting as a competing endogenous RNA to sponge microRNA-142-3p to participate in gemcitabine resistance in pancreatic cancer via upregulating TWF1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102307
                DO  - 10.18632/aging.102307
                SP  - 8860
                EP  - 8878
                PY  - 
                AB  - Objective: This study is implemented to probe into the function of lncRNA SBF2-AS1 as a competing endogenous RNA (ceRNA) to sponge microRNA-142-3p (miR-142-3p) in modulating TWF1 expression in the gemcitabine resistance of pancreatic cancer.Results: LncRNA SBF2-AS1 was highly expressed in pancreatic cancer tissues and cells. SBF2-AS1 was found to be associated with gemcitabine resistance in pancreatic cancer. Knock-down of SBF2-AS1 inhibited proliferation, epithelial-mesenchymal transition, while promoting apoptosis of gemcitabine resistant pancreatic cancer cells. SBF2-AS1 inhibited the expression of TWF1 by competitively binding with miR-142-3p in pancreatic cancer.Conclusion: Our study demonstrates that knock-down of SBF2-AS1 inhibits the expression of TWF1 by competitively binding with miR-142-3p to induce gemcitabine resistance in pancreatic cancer.Methods: Expression of SBF2-AS1 was tested in pancreatic cancer tissues and cells. Construction of AsPC-1/GEM and PANC-1/GEM cells with low expression of SBF2-AS1 was performed to determine the biological behaviors of drug-resistant cells. AsPC-1 and PANC-1 cells expressing SBF2-AS1 and/or miR-142-3p were constructed and treated with different concentrations of gemcitabine to detect the sensitivity of the cells to gemcitabine. The binding relationship between SBF2-AS1 and miR-142-3p and between miR-142-3p and TWF1 were determined.
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CD8+CXCR5+T cells infiltrating hepatocellular carcinomas are activated and predictive of a better prognosis

Linsen Ye, Yang Li, Hui Tang, Wei Liu, Yunhao Chen, Tianxing Dai, Rongpu Liang, Mengchen Shi, Shuhong Yi, Guihua Chen, Yang Yang,

https://doi.org/10.18632/aging.102308 pp 8879—8891

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Ye L, Li Y, Tang H, Liu W, Chen Y, Dai T, Liang R, Shi M, Yi S, Chen G, Yang Y, . CD8+CXCR5+T cells infiltrating hepatocellular carcinomas are activated and predictive of a better prognosis. . 11:8879-8891. https://doi.org/10.18632/aging.102308

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                TY  - JOUR
                AU  - Ye, Linsen 
                AU  - Li, Yang 
                AU  - Tang, Hui 
                AU  - Liu, Wei 
                AU  - Chen, Yunhao 
                AU  - Dai, Tianxing 
                AU  - Liang, Rongpu 
                AU  - Shi, Mengchen 
                AU  - Yi, Shuhong 
                AU  - Chen, Guihua 
                AU  - Yang, Yang 
                TI  - CD8+CXCR5+T cells infiltrating hepatocellular carcinomas are activated and predictive of a better prognosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102308
                DO  - 10.18632/aging.102308
                SP  - 8879
                EP  - 8891
                PY  - 
                AB  - CD8+ T cells are thought to be the primary cytotoxic lymphocytes exerting antitumor effects. However, few studies have focused on the antitumor effects of CD8+ T cell-mediated humoral immunity or on interactions between CD8+ T cells and B cells in hepatocellular carcinoma (HCC). We found that the frequency of IL-21-producing CD8+CXCR5+ T cells was higher in HCC tumor tissue than in peritumoral tissue or peripheral blood from the same patients or in blood from healthy donors. Moreover, CD8+CXCR5+ T cells migrated in response to supernatants from primary HCC (HCC-SN) cells, and HCC-SN cells also powerfully induced CXCR5 expression in CD8+ T cells and IL-21 expression in CD8+CXCR5+ T cells. CD8+CXCR5+ T cells from HCC patients, but not those from healthy individuals, stimulated CD19+ B cells to differentiate into IgG-producing plasmablasts. These findings reveal that CD8+CXCR5+ T cells strongly infiltrate HCC tumors, and their infiltration is predictive of a better prognosis. Surprisingly, moreover, CD8+CXCR5+ T cells produced IL-21, which induced B cells to differentiate into IgG-producing plasmablasts and to play a key role in humoral immunity in HCC.
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TGF-β receptor inhibitor LY2109761 enhances the radiosensitivity of gastric cancer by inactivating the TGF-β/SMAD4 signaling pathway

Tian Yang, Tianhe Huang, Dongdong Zhang, Miao Wang, Balu Wu, Yufeng Shang, Safat Sattar, Lu Ding, Yin Liu, Hongqiang Jiang, Yuxing Liang, Fuling Zhou, Yongchang Wei,

https://doi.org/10.18632/aging.102329 pp 8892—8910

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Yang T, Huang T, Zhang D, Wang M, Wu B, Shang Y, Sattar S, Ding L, Liu Y, Jiang H, Liang Y, Zhou F, Wei Y, . TGF-β receptor inhibitor LY2109761 enhances the radiosensitivity of gastric cancer by inactivating the TGF-β/SMAD4 signaling pathway. . 11:8892-8910. https://doi.org/10.18632/aging.102329

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                TY  - JOUR
                AU  - Yang, Tian 
                AU  - Huang, Tianhe 
                AU  - Zhang, Dongdong 
                AU  - Wang, Miao 
                AU  - Wu, Balu 
                AU  - Shang, Yufeng 
                AU  - Sattar, Safat 
                AU  - Ding, Lu 
                AU  - Liu, Yin 
                AU  - Jiang, Hongqiang 
                AU  - Liang, Yuxing 
                AU  - Zhou, Fuling 
                AU  - Wei, Yongchang 
                TI  - TGF-β receptor inhibitor LY2109761 enhances the radiosensitivity of gastric cancer by inactivating the TGF-β/SMAD4 signaling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102329
                DO  - 10.18632/aging.102329
                SP  - 8892
                EP  - 8910
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yang, Tian 
                AU  - Huang, Tianhe 
                AU  - Zhang, Dongdong 
                AU  - Wang, Miao 
                AU  - Wu, Balu 
                AU  - Shang, Yufeng 
                AU  - Sattar, Safat 
                AU  - Ding, Lu 
                AU  - Liu, Yin 
                AU  - Jiang, Hongqiang 
                AU  - Liang, Yuxing 
                AU  - Zhou, Fuling 
                AU  - Wei, Yongchang 
                TI  - TGF-β receptor inhibitor LY2109761 enhances the radiosensitivity of gastric cancer by inactivating the TGF-β/SMAD4 signaling pathway
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102329
                DO  - 10.18632/aging.102329
                SP  - 8892
                EP  - 8910
                PY  - 
                AB  - Radiotherapy is used to treat gastric cancer (GC); however, radioresistance challenges the clinical outcomes of GC, and the mechanisms of radioresistance in GC remain poorly understood. Here, we report that the TGF-&#x3B2; receptor inhibitor, LY2109761 (LY), is a potential radiosensitizer both in vitro and in vivo. As per the Cancer Genome Atlas database, TGF-&#x3B2; overexpression is significantly related to poor overall survival in GC patients. We demonstrated that the TGF-&#x3B2;/SMAD4 signaling pathway was activated in both radioresistant GC cells and radioresistant GC patients. As a TGF-&#x3B2; receptor inhibitor, LY can enhance the activities of irradiation by inhibiting cell proliferation, decreasing clonogenicity and increasing apoptosis. Moreover, LY attenuated the radiation-induced migration and invasion, epithelial-mesenchymal transition (EMT), inflammatory factor activation, immunosuppression, and cancer stem cell characteristics of GC cells, thus leading to radiosensitization of the GC cells. We confirmed that LY reduced tumor growth, inhibited TGF-&#x3B2;/SMAD4 pathway activation and reversed irradiation-induced EMT in a tumor xenograft model. Our findings indicate that the novel TGF-&#x3B2; receptor inhibitor, LY, increases GC radiosensitivity by directly regulating the TGF-&#x3B2;/SMAD4 signaling pathway. These findings provide new insight for radiotherapy in GC patients.
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Immature dendritic cells derived exosomes promotes immune tolerance by regulating T cell differentiation in renal transplantation

Xin-Lu Pang, Zhi-Gang Wang, Lei Liu, Yong-Hua Feng, Jun-Xiang Wang, Hong-Chang Xie, Xian-Lei Yang, Jin-Feng Li, Gui-Wen Feng,

https://doi.org/10.18632/aging.102346 pp 8911—8924

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Pang X, Wang Z, Liu L, Feng Y, Wang J, Xie H, Yang X, Li J, Feng G, . Immature dendritic cells derived exosomes promotes immune tolerance by regulating T cell differentiation in renal transplantation. . 11:8911-8924. https://doi.org/10.18632/aging.102346

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                TY  - JOUR
                AU  - Pang, Xin-Lu 
                AU  - Wang, Zhi-Gang 
                AU  - Liu, Lei 
                AU  - Feng, Yong-Hua 
                AU  - Wang, Jun-Xiang 
                AU  - Xie, Hong-Chang 
                AU  - Yang, Xian-Lei 
                AU  - Li, Jin-Feng 
                AU  - Feng, Gui-Wen 
                TI  - Immature dendritic cells derived exosomes promotes immune tolerance by regulating T cell differentiation in renal transplantation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102346
                DO  - 10.18632/aging.102346
                SP  - 8911
                EP  - 8924
                PY  - 
                AB  - Objective: To investigate the mechanism of immature dendritic cells-derived exosomes (imDECs) in the regulation of T cell differentiation and immune tolerance in renal allograft model mice.Results: imDECs significantly improved the percent of survival, relieved inflammatory response, and reduced CD4+T cell infiltration. In addition, imDECs reduced the rejection associated cytokines in allograft mice, and increased the percentage of Foxp3+CD4+T cells in spleen and kidney tissues. imDECs suppressed the IL17+CD4+T cells and promoted the Foxp3+CD4+T cells under Th17 polarization condition. Moreover, miR-682 was found to be highly expressed in imDECs which suppressed the IL17+CD4+T cells and promoted the Foxp3+CD4+T cells. Luciferase reporter assay showed ROCK2 was a target of miR-682, and ROCK mRNA level was negative correlated with miR-682 mRNA level.Conclusion: miR-682 was highly expressed in imDECs, and imDECs-secreted miR-682 promoted Treg cell differentiation by negatively regulating ROCK2 to promote immune tolerance in renal allograft model mice.Methods: Renal allograft model mice were established, and imDECs or mature dendritic cells-derived exosomes (mDECs) were injected into model mice. Rejection associated cytokines IFN-&#x3B3;, IL-2, IL-17 levels in plasma were detected by ELISA. IL-17A, Foxp3, miR-682, ROCK2, p-STAT3, p-STAT5 expressions were measured by qRT-PCR or western blot.
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Short-term efficacy of ticagrelor in acute ST-segment elevation myocardial infarction patients undergoing an emergency percutaneous coronary intervention

Bangming Cao, Fuzheng Qu, Xianliang Liu, Changzheng Gao, Qiang Fu, Chunying Jiang, Peng Wei, Qianqian Ma,

https://doi.org/10.18632/aging.102353 pp 8925—8936

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Cao B, Qu F, Liu X, Gao C, Fu Q, Jiang C, Wei P, Ma Q, . Short-term efficacy of ticagrelor in acute ST-segment elevation myocardial infarction patients undergoing an emergency percutaneous coronary intervention. . 11:8925-8936. https://doi.org/10.18632/aging.102353

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                TY  - JOUR
                AU  - Cao, Bangming 
                AU  - Qu, Fuzheng 
                AU  - Liu, Xianliang 
                AU  - Gao, Changzheng 
                AU  - Fu, Qiang 
                AU  - Jiang, Chunying 
                AU  - Wei, Peng 
                AU  - Ma, Qianqian 
                TI  - Short-term efficacy of ticagrelor in acute ST-segment elevation myocardial infarction patients undergoing an emergency percutaneous coronary intervention
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102353
                DO  - 10.18632/aging.102353
                SP  - 8925
                EP  - 8936
                PY  - 
                AB  - In total, 97 acute ST-segment elevation myocardial infarction (STEMI) patients who received an emergency percutaneous coronary intervention (PCI) were enrolled and divided into a ticagrelor group and a clopidogrel group. Thrombolysis in myocardial infarction (TIMI) blood flow and the corrected TIMI frame count (CTFC) were used to assess the blood perfusion of culprit vessels. Thromboelastography (TEG) was used to evaluate the antiplatelet effect of drugs. The results showed that the incidence of TIMI grade III blood flow in the ticagrelor group was significantly higher than that in the clopidogrel group. The CTFC in the anterior descending, circumflex, and right coronary arteries was statistically significantly lower in the ticagrelor group as compared with that in the clopidogrel group. At 2 h and 7 d postdrug treatment, the adenosine diphosphate-induced platelet inhibition rate (ADP%) in the ticagrelor group increased significantly as compared with that in the clopidogrel group, and the platelet aggregation rate of the ADP pathway (MAADP) decreased significantly in the ticagrelor group versus that in the clopidogrel group. In conclusion, ticagrelor significantly improved TIMI blood flow and had a better antiplatelet effect than clopidogrel in STEMI patients undergoing an emergency PCI.
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Beneficial effects of PGC-1α in the substantia nigra of a mouse model of MPTP-induced dopaminergic neurotoxicity

Yingqing Wang, Chun Chen, Wanling Huang, Maoxin Huang, Juhua Wang, Xiaochun Chen, Qinyong Ye,

https://doi.org/10.18632/aging.102357 pp 8937—8950

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Wang Y, Chen C, Huang W, Huang M, Wang J, Chen X, Ye Q, . Beneficial effects of PGC-1α in the substantia nigra of a mouse model of MPTP-induced dopaminergic neurotoxicity. . 11:8937-8950. https://doi.org/10.18632/aging.102357

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                TY  - JOUR
                AU  - Wang, Yingqing 
                AU  - Chen, Chun 
                AU  - Huang, Wanling 
                AU  - Huang, Maoxin 
                AU  - Wang, Juhua 
                AU  - Chen, Xiaochun 
                AU  - Ye, Qinyong 
                TI  - Beneficial effects of PGC-1α in the substantia nigra of a mouse model of MPTP-induced dopaminergic neurotoxicity
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102357
                DO  - 10.18632/aging.102357
                SP  - 8937
                EP  - 8950
                PY  - 
                AB  - Background: Mitochondrial dysfunction and oxidative stress are closely associated with the pathogenesis of Parkinson&#x2019;s disease. Peroxisome proliferator-activated receptor &#x3B3; coactivator 1 alpha (PGC-1&#x3B1;) is thought to play multiple roles in the regulation of mitochondrial biogenesis and cellular energy metabolism. We recently reported that altering PGC-1&#x3B1; gene expression modulates mitochondrial functions in N-methyl-4-phenylpyridinium ion (MPP+) treated human SH-SY5Y neuroblastoma cells, possibly via the regulation of Estrogen-related receptor &#x3B1; (ERR&#x3B1;), nuclear respiratory factor 1 (NRF-1), nuclear respiratory factor 2 (NRF-2) and peroxisome proliferator-activated receptor &#x3B3; (PPAR&#x3B3;) expression. In the present study, we aimed to further investigate the potential beneficial effects of PGC-1&#x3B1; in the substantia nigra of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated C57BL mice.Methods: The overexpression or knockdown of the PGC-1&#x3B1; gene in the mouse model of dopaminergic neurotoxicity was performed using a stereotactic injection of lentivirus in MPTP-treated male C57BL/6 mice. Mice were randomly assigned to one of 6 groups (n=24 per group): normal saline (NS) intraperitoneal injection (i.p.) (con); MPTP i.p. (M); solvent of the lentivirus striatal injection (lentivirus control) + MPTP i.p. (LVcon+M); lentivirus striatal injection + MPTP i.p. (LV+M); LV-PGC-1&#x3B1; striatum injection + MPTP i.p. (LVPGC+M); and LV-PGC-1&#x3B1;-siRNA striatal injection + MPTP i.p. (LVsiRNA+M). Intraperitoneal injections of MPTP/NS were conducted two weeks after lentivirus injection.Results: We found significant improvement in motor behavior and increases in tyrosine hydroxylase expression in the substantia nigra (SN) in the brains of mice in the LVPGC+M group. The opposite tendency was observed in those in the LVsiRNA+M group. The expression of superoxide dismutase (SOD) in the SN region was also consistent with the changes in PGC-1&#x3B1; expression. Electron microscopy showed an increasing trend in the mitochondrial density in the LVPGC+M group and a decreasing trend in the M and LVsiRNA+M groups compared to that in the controls.Conclusions: Our results indicated that PGC-1&#x3B1; rescues the effects of MPTP-induced mitochondrial dysfunction in C57BL mice.
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LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer

Yucai Wei, Fan Zhang, Tong Zhang, Yating Zhang, Hao Chen, Furong Wang, Yumin Li,

https://doi.org/10.18632/aging.102359 pp 8951—8968

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Wei Y, Zhang F, Zhang T, Zhang Y, Chen H, Wang F, Li Y, . LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer. . 11:8951-8968. https://doi.org/10.18632/aging.102359

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                TY  - JOUR
                AU  - Wei, Yucai 
                AU  - Zhang, Fan 
                AU  - Zhang, Tong 
                AU  - Zhang, Yating 
                AU  - Chen, Hao 
                AU  - Wang, Furong 
                AU  - Li, Yumin 
                TI  - LDLRAD2 overexpression predicts poor prognosis and promotes metastasis by activating Wnt/β-catenin/EMT signaling cascade in gastric cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102359
                DO  - 10.18632/aging.102359
                SP  - 8951
                EP  - 8968
                PY  - 
                AB  - The therapeutic strategies for advanced gastric cancer (GC) remain unsatisfying and limited. Therefore, it is still imperative to fully elucidate the mechanisms underlying GC aggressive progression. The prognostic value and biological functions of low density lipoprotein receptor class A domain containing protein 2 (LDLRAD2) in GC have never been studied yet. We found that LDLRAD2 expression was significantly upregulated in GC and closely correlated with poor prognosis in GC patients. Functionally, LDLRAD2 promoted epithelial-mesenchymal transition, migration and invasion, and metastasis of GC cells. Mechanistically, LDLRAD2 interacted with and inhibited Axin1 from binding to cytoplasmic &#x3B2;-catenin, which facilitated the nuclear translocation of &#x3B2;-catenin, thereby activating Wnt/&#x3B2;-catenin pathway. Inhibition of &#x3B2;-catenin activity markedly abolished LDLRAD2-induced migration, invasion and metastasis. Together, these results suggested that LDLRAD2 contributed to invasion and metastasis of GC through activating Wnt/&#x3B2;-catenin pathway. LDLRAD2/ Wnt/&#x3B2;-catenin axis may be a potential therapeutic target for GC treatment.
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Expression and significance of miR - 20b in retinal photoreceptor cells exposed to PCB₁₂₅₄

Xin Zhang, Qingyu Zhang, Yue Jiang, Shuchun Zhang, Qin Hong, Xirong Guo, Xia Chi, Meiling Tong,

https://doi.org/10.18632/aging.102360 pp 8969—8981

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Zhang X, Zhang Q, Jiang Y, Zhang S, Hong Q, Guo X, Chi X, Tong M, . Expression and significance of miR - 20b in retinal photoreceptor cells exposed to PCB₁₂₅₄. . 11:8969-8981. https://doi.org/10.18632/aging.102360

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                TY  - JOUR
                AU  - Zhang, Xin 
                AU  - Zhang, Qingyu 
                AU  - Jiang, Yue 
                AU  - Zhang, Shuchun 
                AU  - Hong, Qin 
                AU  - Guo, Xirong 
                AU  - Chi, Xia 
                AU  - Tong, Meiling 
                TI  - Expression and significance of miR - 20b in retinal photoreceptor cells exposed to PCB<sub>1254</sub>
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102360
                DO  - 10.18632/aging.102360
                SP  - 8969
                EP  - 8981
                PY  - 
                AB  - Previous studies have shown that PCB1254 has an adverse effect on zebrafish retinal development, but the basic mechanism behind it is not clear. The purpose of this study was to investigate the molecular mechanisms of PCB-induced retinal dysplasia. RT-qPCR, immunoblotting, HE staining and immunofluorescence were adopted to detect the expression at mRNA and protein level. Functional experiments were carried out in 661w cells including CCK-8 assay, caspase-3 assay, and the flow cytometry, while the functional role of miR - 20b was further investigated by using the zebrafish model. The result showed that PCB1254 exposure inhibited cell proliferation and increased the apoptosis of the 661w cells, and the dose&#x2013;response relationship between the retinal development-related genes (SWS1, CRX, Rho), miR-20b expression and PCB1254 exposure was also discovered. We confirmed that miR-20b targeted FGF2 and GRB2 by constructing a dual luciferase reporter gene and suppressed the cell function as well as PCB1254. In the miR-20b overexpression zebrafish model, we found abnormal retinal morphology characterized by sparse and irregular photoreceptor cells and the thick photoreceptor cell layers. Our results demonstrate for the first time that PCBs target the MAPK/ERK signaling through miR-20b, affecting retinal cell development and leading to visual impairment.
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Heat shock factor 1-mediated transcription activation of Omi/HtrA2 induces myocardial mitochondrial apoptosis in the aging heart

Dan Liu, Linguo Wu, Ye Wu, Xin Wei, Wen Wang, Suli Zhang, Ming Yi, Jing Li, Huirong Liu, Xinliang Ma,

https://doi.org/10.18632/aging.102361 pp 8982—8997

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Liu D, Wu L, Wu Y, Wei X, Wang W, Zhang S, Yi M, Li J, Liu H, Ma X, . Heat shock factor 1-mediated transcription activation of Omi/HtrA2 induces myocardial mitochondrial apoptosis in the aging heart. . 11:8982-8997. https://doi.org/10.18632/aging.102361

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                TY  - JOUR
                AU  - Liu, Dan 
                AU  - Wu, Linguo 
                AU  - Wu, Ye 
                AU  - Wei, Xin 
                AU  - Wang, Wen 
                AU  - Zhang, Suli 
                AU  - Yi, Ming 
                AU  - Li, Jing 
                AU  - Liu, Huirong 
                AU  - Ma, Xinliang 
                TI  - Heat shock factor 1-mediated transcription activation of Omi/HtrA2 induces myocardial mitochondrial apoptosis in the aging heart
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102361
                DO  - 10.18632/aging.102361
                SP  - 8982
                EP  - 8997
                PY  - 
                AB  - Background: Increased cardiac apoptosis is a hallmark of the elderly, which in turn increases the risk for developing cardiac disease. The overexpression of Omi/HtrA2 mRNA and protein contributes to apoptosis in the aged heart. Heat shock factor 1 (HSF1) is a transcription factor that binds to the promoter of Omi/HtrA2 in the aging myocardium. However, whether HSF1 participates in cardiomyocyte apoptosis via transcriptional regulation of Omi/HtrA2 remains unclear. The present study was designed to investigate whether HSF1 plays a role in Omi/HtrA2 transcriptional regulation and myocardial apoptosis.Methods and Results: Assessment of the hearts of mice of different ages was performed, which indicated a decrease in cardiac function reserve and an increase in mitochondrial apoptosis. Omi/HtrA2 overexpression in the elderly was negatively correlated with left ventricular function after exercise overload and positively correlated with myocardial Caspase-9 apoptosis. Chromatin immunoprecipitation (ChIP) of aging hearts and plasmid transfection/RNA interference of H9C2 cells revealed that enhancement of HSF1 expression promotes Omi/HtrA2 expression by inducing the promoter activity of Omi/HtrA2 while also increasing mitochondrial apoptosis by upregulating Omi/HtrA2 expression.Conclusions: HSF1 acts as a transcriptional factor that induces Omi/HtrA2 expression and Caspase-9 apoptosis in aged cardiomyocytes, while also decreasing cardiac function reserve.
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TIMP1 mRNA in tumor-educated platelets is diagnostic biomarker for colorectal cancer

Liu Yang, Qian Jiang, Dong-Zheng Li, Xin Zhou, Dong-Sheng Yu, Jian Zhong,

https://doi.org/10.18632/aging.102366 pp 8998—9012

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Yang L, Jiang Q, Li D, Zhou X, Yu D, Zhong J, . TIMP1 mRNA in tumor-educated platelets is diagnostic biomarker for colorectal cancer. . 11:8998-9012. https://doi.org/10.18632/aging.102366

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                TY  - JOUR
                AU  - Yang, Liu 
                AU  - Jiang, Qian 
                AU  - Li, Dong-Zheng 
                AU  - Zhou, Xin 
                AU  - Yu, Dong-Sheng 
                AU  - Zhong, Jian 
                TI  - TIMP1 mRNA in tumor-educated platelets is diagnostic biomarker for colorectal cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102366
                DO  - 10.18632/aging.102366
                SP  - 8998
                EP  - 9012
                PY  - 
                AB  - Platelets have been shown to promote the growth of tumors, including colorectal cancer. The RNA profile of tumor-educated platelets has the possibility for cancer diagnosis. We used RNA sequencing to identified the gene expression signature in platelets from colorectal cancer patients and healthy volunteers. We then verified the selected biomarkers from the RNA sequencing in a two-step case-control study using quantitative reverse-transcription polymerase chain reaction. We found that TIMP1 mRNA levels are higher in platelets from colorectal cancer patients than in platelets from healthy volunteers and patients with inflammatory bowel diseases. Additionally, TIMP1 mRNA expressed in platelets from colorectal cancer patients can be carried into colorectal cancer cells, where it promotes tumor growth in vivo and in vitro. These findings show that the TIMP1 mRNA in platelets is a potential independent diagnostic biomarker for colorectal cancer, and that platelets can carry RNAs into colorectal cancer cells to promote colorectal cancer development.
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Melatonin induces progesterone production in human granulosa-lutein cells through upregulation of StAR expression

Lanlan Fang, Yiran Li, Sijia Wang, Yiping Yu, Yuxi Li, Yanjie Guo, Yang Yan, Ying-Pu Sun,

https://doi.org/10.18632/aging.102367 pp 9013—9024

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Fang L, Li Y, Wang S, Yu Y, Li Y, Guo Y, Yan Y, Sun Y, . Melatonin induces progesterone production in human granulosa-lutein cells through upregulation of StAR expression. . 11:9013-9024. https://doi.org/10.18632/aging.102367

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                TY  - JOUR
                AU  - Fang, Lanlan 
                AU  - Li, Yiran 
                AU  - Wang, Sijia 
                AU  - Yu, Yiping 
                AU  - Li, Yuxi 
                AU  - Guo, Yanjie 
                AU  - Yan, Yang 
                AU  - Sun, Ying-Pu 
                TI  - Melatonin induces progesterone production in human granulosa-lutein cells through upregulation of StAR expression
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102367
                DO  - 10.18632/aging.102367
                SP  - 9013
                EP  - 9024
                PY  - 
                AB  - Steroidogenic acute regulatory protein (StAR) mediates the rate-limiting step in ovarian steroidogenesis and progesterone (P4) synthesis. Melatonin and its receptors are expressed in human granulosa cells, and have been shown to influence basal P4 production. However, previous studies addressing the regulation of StAR expression by melatonin and its impact on P4 secretion yielded contradictory results. Here, we demonstrate that melatonin upregulates StAR expression in primary cultures of human granulosa-lutein (hGL) cells obtained from women undergoing in vitro fertilization (IVF). Using pharmacological inhibitors, we show that the stimulatory effect of melatonin on StAR expression is mediated via both MT1 and MT2 melatonin receptors. Melatonin exposure activates the PI3K/AKT signaling pathway and its inhibition attenuates the stimulatory effect of melatonin on StAR expression. Moreover, siRNA-mediated knockdown of StAR abolishes melatonin-induced P4 production. Importantly, clinical analyses demonstrate that melatonin levels in human follicular fluid are positively correlated with P4 levels in serum. By illustrating the potential physiological role of melatonin in the regulation of StAR expression and P4 production in hGL cells, our results may serve to improve current strategies used to treat clinical infertility.
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Differentially expressed autophagy-related genes are potential prognostic and diagnostic biomarkers in clear-cell renal cell carcinoma

Bangbei Wan, Bo Liu, Gang Yu, Yuan Huang, Cai Lv,

https://doi.org/10.18632/aging.102368 pp 9025—9042

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Wan B, Liu B, Yu G, Huang Y, Lv C, . Differentially expressed autophagy-related genes are potential prognostic and diagnostic biomarkers in clear-cell renal cell carcinoma. . 11:9025-9042. https://doi.org/10.18632/aging.102368

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                TY  - JOUR
                AU  - Wan, Bangbei 
                AU  - Liu, Bo 
                AU  - Yu, Gang 
                AU  - Huang, Yuan 
                AU  - Lv, Cai 
                TI  - Differentially expressed autophagy-related genes are potential prognostic and diagnostic biomarkers in clear-cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102368
                DO  - 10.18632/aging.102368
                SP  - 9025
                EP  - 9042
                PY  - 
                AB  - We examined the role of differentially expressed autophagy-related genes (DEARGs) in clear cell Renal Cell Carcinoma (ccRCC) using high-throughput RNA-seq data from The Cancer Genome Atlas (TCGA). Cox regression analyses showed that 5 DEARGs (PRKCQ, BID, BAG1, BIRC5, and ATG16L2) correlated with overall survival (OS) and 4 DEARGs (EIF4EBP1, BAG1, ATG9B, and BIRC5) correlated with disease-free survival (DFS) in ccRCC patients. Multivariate Cox regression analysis using the OS and DFS prognostic risk models showed that expression of the nine DEARGs accurately and independently predicted the risk of disease recurrence or progression in ccRCC patients (area under curve or AUC values &gt; 0.70; all p &lt; 0.05). Moreover, the DEARGs accurately distinguished healthy individuals from ccRCC patients based on receiver operated characteristic (ROC) analyses (area under curve or AUC values &gt; 0.60), suggesting their potential as diagnostic biomarkers for ccRCC. The expression of DEARGs also correlated with the drug sensitivity of ccRCC cell lines. The ccRCC cell lines were significantly sensitive to Sepantronium bromide, a drug that targets BIRC5. This makes BIRC5 a potential therapeutic target for ccRCC. Our study thus demonstrates that DEARGs are potential diagnostic and prognostic biomarkers and therapeutic targets in ccRCC.
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T5224, RSPO2 and AZD5363 are novel drugs against functional pituitary adenoma

Sheng Zhong, Bo Wu, Jiahui Li, Xinhui Wang, Shanshan Jiang, Fangfei Hu, Gaojing Dou, Yuan Zhang, Chunjia Sheng, Gang Zhao, Yunqian Li, Yong Chen,

https://doi.org/10.18632/aging.102372 pp 9043—9059

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Zhong S, Wu B, Li J, Wang X, Jiang S, Hu F, Dou G, Zhang Y, Sheng C, Zhao G, Li Y, Chen Y, . T5224, RSPO2 and AZD5363 are novel drugs against functional pituitary adenoma. . 11:9043-9059. https://doi.org/10.18632/aging.102372

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                TY  - JOUR
                AU  - Zhong, Sheng 
                AU  - Wu, Bo 
                AU  - Li, Jiahui 
                AU  - Wang, Xinhui 
                AU  - Jiang, Shanshan 
                AU  - Hu, Fangfei 
                AU  - Dou, Gaojing 
                AU  - Zhang, Yuan 
                AU  - Sheng, Chunjia 
                AU  - Zhao, Gang 
                AU  - Li, Yunqian 
                AU  - Chen, Yong 
                TI  - T5224, RSPO2 and AZD5363 are novel drugs against functional pituitary adenoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102372
                DO  - 10.18632/aging.102372
                SP  - 9043
                EP  - 9059
                PY  - 
                AB  - We tested whether the drugs T5224, RSPO2, and AZD5363 exert therapeutic effects against functioning pituitary adenoma (FPA). We analysed the gene expression profiles of four FPA mRNA microarray datasets (GSE2175, GSE26966, GSE36314, and GSE37153) from the Gene Expression Omnibus database and identified genes differentially expressed in FPA vs control tissues. We then carried out Gene Ontology, Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction network analyses. We also measured the difference in expression of hub genes between human normal pituitary cells and FPA cells using qRT-PCR. Our in vitro colony-formation and MTT assays showed that cell viability, number, and the size of clonogenicities were all lower in the presence of T5224, RSPO2, or AZD536 than in controls. Moreover, flow cytometry experiments showed that the incidence of apoptosis was higher in the presence of T5224, RSPO2, or AZD5363 than among controls, and was increased by increasing the doses of the drugs. This suggests these drugs could be used as therapeutic agents to treat FPA. Finally, we found that cFos, WNT5A, NCAM1, JUP, AKT3, and ADCY1 are abnormally expressed in FPA cells compared to controls, which highlights these genes as potential prognostic and/or therapeutic targets.
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Age-dependent relationship between preoperative serum aminotransferase and mortality after cardiovascular surgery

Jae-Sik Nam, Wook-Jong Kim, Sang-Mee An, Dae-Kee Choi, Ji-Hyun Chin, Eun-Ho Lee, In-Cheol Choi,

https://doi.org/10.18632/aging.102374 pp 9060—9074

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Nam J, Kim W, An S, Choi D, Chin J, Lee E, Choi I, . Age-dependent relationship between preoperative serum aminotransferase and mortality after cardiovascular surgery. . 11:9060-9074. https://doi.org/10.18632/aging.102374

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                TY  - JOUR
                AU  - Nam, Jae-Sik 
                AU  - Kim, Wook-Jong 
                AU  - An, Sang-Mee 
                AU  - Choi, Dae-Kee 
                AU  - Chin, Ji-Hyun 
                AU  - Lee, Eun-Ho 
                AU  - Choi, In-Cheol 
                TI  - Age-dependent relationship between preoperative serum aminotransferase and mortality after cardiovascular surgery
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102374
                DO  - 10.18632/aging.102374
                SP  - 9060
                EP  - 9074
                PY  - 
                AB  - Although serum aminotransferase levels are frequently measured for preoperative evaluation, their prognostic value to postoperative outcomes remain unclear. This study aimed to investigate the relationship between preoperative serum aminotransferase levels and postoperative 90-day mortality in patients undergoing cardiovascular surgery. We included adult patients (n=6264) who underwent cardiovascular surgery between January 2010 and December 2016 at a tertiary academic hospital. Preoperative serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST), and De Ritis ratio (defined as AST/ALT) were categorized into three groups: low (&#x2264;20th percentile), middle (20th&#x2013;80th percentile), and high (&gt;80th percentile). Of the 6264 patients enrolled (40.4% women; median age, 62 years), 183 (2.9%) died within 90 days postoperatively. Multivariable-adjusted analyses revealed low ALT (hazard ratio 1.58, 95% confidence interval, 1.14&#x2013;2.18) and high De Ritis ratio (hazard ratio 1.59, 95% confidence interval, 1.15&#x2013;2.20) were independent predictors of postoperative mortality, but AST did not have a statistically significant association. The association of low ALT and high De Ritis ratio with 90-day mortality was more pronounced in patients older than 60 years (P-values for interaction &lt;0.05). Therefore, preoperative serum aminotransferase levels may be a valuable prognostic marker in patients with cardiovascular surgery, particularly in the elderly.
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Sirtuin 3 attenuates neuroinflammation-induced apoptosis in BV-2 microglia

Dingzhou Zhou, Yugang Jiang,

https://doi.org/10.18632/aging.102375 pp 9075—9089

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Zhou D, Jiang Y, . Sirtuin 3 attenuates neuroinflammation-induced apoptosis in BV-2 microglia. . 11:9075-9089. https://doi.org/10.18632/aging.102375

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                TY  - JOUR
                AU  - Zhou, Dingzhou 
                AU  - Jiang, Yugang 
                TI  - Sirtuin 3 attenuates neuroinflammation-induced apoptosis in BV-2 microglia
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102375
                DO  - 10.18632/aging.102375
                SP  - 9075
                EP  - 9089
                PY  - 
                AB  - In this study, we explored the upstream regulatory mechanisms underlying inflammation-induced mitochondrial dysfunction in microglial BV-2 cells. Our results demonstrate that Sirtuin 3 (Sirt3) expression was downregulated in response to LPS-induced neuroinflammation. In addition, overexpression of Sirt3 attenuated LPS-induced BV-2 cell death. Functional studies illustrated that Sirt3 overexpression promoted normal mitochondrial function and inhibited mitochondria-dependent apoptosis in LPS-treated BV-2 cells. At the molecular level, suppressor of ras val-2 (SRV2) promoted LPS-mediated mitochondrial damage by inducing mitochondrial fission. Sirt3 overexpression, which suppressed the transcription of SRV2 and thus suppressed mitochondrial fission, played an anti-apoptotic role in LPS-treated BV-2 cells. Furthermore, Sirt3 inhibited SRV2 expression via the Mst1-JNK pathway, and re-activation of this pathway abolished the protective effects of Sirt3 on mitochondrial damage and apoptosis. Taken together, our results indicate that Sirt3-induced, Mst1-JNK-SRV2 signaling pathway-dependent inhibition of mitochondrial fission protected against neuroinflammation-mediated cell damage in BV-2 microglia. Sirt3 might therefore be an effective treatment for neuroinflammation.
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Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16

Guohua Zhang, Ying Xu, Chen Zou, Yinbing Tang, Jiawei Lu, Zhigang Gong, Gui Ma, Wenbo Zhang, Pengcheng Jiang,

https://doi.org/10.18632/aging.102377 pp 9090—9110

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Zhang G, Xu Y, Zou C, Tang Y, Lu J, Gong Z, Ma G, Zhang W, Jiang P, . Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16. . 11:9090-9110. https://doi.org/10.18632/aging.102377

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                TY  - JOUR
                AU  - Zhang, Guohua 
                AU  - Xu, Ying 
                AU  - Zou, Chen 
                AU  - Tang, Yinbing 
                AU  - Lu, Jiawei 
                AU  - Gong, Zhigang 
                AU  - Ma, Gui 
                AU  - Zhang, Wenbo 
                AU  - Jiang, Pengcheng 
                TI  - Long noncoding RNA ARHGAP27P1 inhibits gastric cancer cell proliferation and cell cycle progression through epigenetically regulating p15 and p16
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102377
                DO  - 10.18632/aging.102377
                SP  - 9090
                EP  - 9110
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) have emerged as important regulators in the development and progression of gastric cancer (GC). ARHGAP27P1 is a pseudogene-derived lncRNA, and it has been found to be associated with GC in our preliminary study, but this association has not been studied further. Herein, we confirmed that ARHGAP27P1 was significantly downregulated in GC tissues, plasma and cells. Low expression of ARHGAP27P1 was closely associated with advanced TNM stage, increased invasion depth and lymphatic metastasis. Low ARHGAP27P1 expression also predicted a poor prognosis in GC patients. Functionally, overexpression of ARHGAP27P1 inhibited proliferation, invasion, and migration in GC cells, while silencing of ARHGAP27P1 showed the opposite effects. Mechanistic investigations showed that ARHGAP27P1 had a key role in G0/G1 arrest. We further demonstrated that ARHGAP27P1 was associated with Jumonji-domain containing 3 (JMJD3) and that this association was required for the demethylation of H3K27me3, thereby epigenetically activating expression of p15, p16 and p57. Moreover, knockdown of JMJD3, p15, or p16 consistently reversed the inhibitory effects of ARHGAP27P1 in cell proliferation and cell cycle progression. Taken together, these results suggest that lncRNA ARHGAP27P1, as a novel cell cycle regulator, may serve as a potential target for GC prevention and treatment in human GC.
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Long noncoding RNA HULC promotes hepatocellular carcinoma progression

Hongwei Zhang, Zhibin Liao, Furong Liu, Chen Su, He Zhu, Yani Li, Ran Tao, Huifang Liang, Bixiang Zhang, Xuewu Zhang,

https://doi.org/10.18632/aging.102378 pp 9111—9127

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Zhang H, Liao Z, Liu F, Su C, Zhu H, Li Y, Tao R, Liang H, Zhang B, Zhang X, . Long noncoding RNA HULC promotes hepatocellular carcinoma progression. . 11:9111-9127. https://doi.org/10.18632/aging.102378

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                TY  - JOUR
                AU  - Zhang, Hongwei 
                AU  - Liao, Zhibin 
                AU  - Liu, Furong 
                AU  - Su, Chen 
                AU  - Zhu, He 
                AU  - Li, Yani 
                AU  - Tao, Ran 
                AU  - Liang, Huifang 
                AU  - Zhang, Bixiang 
                AU  - Zhang, Xuewu 
                TI  - Long noncoding RNA HULC promotes hepatocellular carcinoma progression
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102378
                DO  - 10.18632/aging.102378
                SP  - 9111
                EP  - 9127
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) are overexpressed in many types of cancers, suggesting they may promote tumorigenesis. The lncRNA &#x201C;highly upregulated in liver cancer&#x201D; (HULC) promotes hepatocellular carcinoma (HCC) by mechanisms that are not fully understood. In the present study, we showed that HULC is overexpressed in HCC tissues, which correlates with an unfavorable prognosis in HCC patients. We also found that HULC promotes the proliferation, migration, and invasion of HCC cells in vitro, and xenograft tumor growth in vivo. Our mechanistic studies showed that HULC works as a competing endogenous RNA for miR-2052, and that the MET receptor tyrosine kinase is a downstream target of miR-2052 in HCC. Furthermore, HULC inhibits miR-2052, thereby stimulating MET expression in HCC. Finally, MET overexpression reverses the effects of HULC depletion. In sum, our findings reveal a novel regulatory signaling cascade, the HULC/miR-2052/MET axis, which could potentially be exploited for therapeutic benefits in the treatment of HCC.
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Mesenchymal stem cell senescence alleviates their intrinsic and seno-suppressive paracrine properties contributing to osteoarthritis development

Olivier Malaise, Yassin Tachikart, Michael Constantinides, Marcus Mumme, Rosanna Ferreira-Lopez, Sandra Noack, Christian Krettek, Daniele Noël, Jing Wang, Christian Jorgensen, Jean-Marc Brondello,

https://doi.org/10.18632/aging.102379 pp 9128—9146

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Malaise O, Tachikart Y, Constantinides M, Mumme M, Ferreira-Lopez R, Noack S, Krettek C, Noël D, Wang J, Jorgensen C, Brondello J, . Mesenchymal stem cell senescence alleviates their intrinsic and seno-suppressive paracrine properties contributing to osteoarthritis development. . 11:9128-9146. https://doi.org/10.18632/aging.102379

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                TY  - JOUR
                AU  - Malaise, Olivier 
                AU  - Tachikart, Yassin 
                AU  - Constantinides, Michael 
                AU  - Mumme, Marcus 
                AU  - Ferreira-Lopez, Rosanna 
                AU  - Noack, Sandra 
                AU  - Krettek, Christian 
                AU  - Noël, Daniele 
                AU  - Wang, Jing 
                AU  - Jorgensen, Christian 
                AU  - Brondello, Jean-Marc 
                TI  - Mesenchymal stem cell senescence alleviates their intrinsic and seno-suppressive paracrine properties contributing to osteoarthritis development
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102379
                DO  - 10.18632/aging.102379
                SP  - 9128
                EP  - 9146
                PY  - 
                AB  - Tissue accumulation of p16INK4a-positive senescent cells is associated with age-related disorders, such as osteoarthritis (OA). These cell-cycle arrested cells affect tissue function through a specific secretory phenotype. The links between OA onset and senescence remain poorly described. Using experimental OA protocol and transgenic Cdkn2a+/luc and Cdkn2aluc/luc mice, we found that the senescence-driving p16INK4a is a marker of the disease, expressed by the synovial tissue, but is also an actor: its somatic deletion partially protects against cartilage degeneration. We test whether by becoming senescent, the mesenchymal stromal/stem cells (MSCs), found in the synovial tissue and sub-chondral bone marrow, can contribute to OA development. We established an in vitro p16INK4a-positive senescence model on human MSCs. Upon senescence induction, their intrinsic stem cell properties are altered. When co-cultured with OA chondrocytes, senescent MSC show also a seno-suppressive properties impairment favoring tissue degeneration. To evaluate in vivo the effects of p16INK4a-senescent MSC on healthy cartilage, we rely on the SAMP8 mouse model of accelerated senescence that develops spontaneous OA. MSCs isolated from these mice expressed p16INK4a. Intra-articular injection in 2-month-old C57BL/6JRj male mice of SAMP8-derived MSCs was sufficient to induce articular cartilage breakdown. Our findings reveal that senescent p16INK4a-positive MSCs contribute to joint alteration.
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Dysfunctional interactions between the default mode network and the dorsal attention network in subtypes of amnestic mild cognitive impairment

Junkai Wang, Jianghong Liu, Zhiqun Wang, Pei Sun, Kuncheng Li, Peipeng Liang,

https://doi.org/10.18632/aging.102380 pp 9147—9166

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Wang J, Liu J, Wang Z, Sun P, Li K, Liang P, . Dysfunctional interactions between the default mode network and the dorsal attention network in subtypes of amnestic mild cognitive impairment. . 11:9147-9166. https://doi.org/10.18632/aging.102380

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                TY  - JOUR
                AU  - Wang, Junkai 
                AU  - Liu, Jianghong 
                AU  - Wang, Zhiqun 
                AU  - Sun, Pei 
                AU  - Li, Kuncheng 
                AU  - Liang, Peipeng 
                TI  - Dysfunctional interactions between the default mode network and the dorsal attention network in subtypes of amnestic mild cognitive impairment
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102380
                DO  - 10.18632/aging.102380
                SP  - 9147
                EP  - 9166
                PY  - 
                AB  - An anticorrelated relationship in the spontaneous fluctuations between the default mode network (DMN) and dorsal attention network (DAN) is a robust feature of intrinsic brain organization in healthy individuals. Prior studies have reported a decreased anticorrelation between the DMN and the DAN in Alzheimer&apos;s disease (AD) and mild cognitive impairment (MCI). However, it is unclear how this anticorrelation changes as MCI progresses to AD. We hypothesized that dysfunctional connectivity between the DMN and DAN may reflect the gradual decline from MCI to AD. To test this hypothesis, we investigated alterations in functional connectivity between the DMN and DAN in subtypes of amnestic MCI (aMCI) by comparing with the same functional pattern in healthy elderly individuals and patients with AD. We retrospectively collected brain imaging and neuropsychological data from 20 AD participants, 22 participants with multiple-domain aMCI (aMCI-m), 29 participants with single-domain aMCI (aMCI-s) and 23 sex-matched normal controls in this study. Resting-state functional connectivity analysis revealed that aMCI-s and aMCI-m groups demonstrated different magnitudes of increased anticorrelation between the DMN and DAN relative to the AD group. Furthermore, in aMCI-s, aMCI-m and AD participants, hypoconnectivity was found in specific regions within the DMN, including the precuneus and angular gyrus, and hyperconnectivity was found in areas outside the typical DMN networks, including the middle occipital gyrus, lingual gyrus and visual cortex, which indicated disease-related adaptations of brain networks. Our findings suggest that DMN-DAN anticorrelation may shed light on the understanding of the adaptations in brain function during the progression from MCI to AD and may serve as a potential biomarker to detect AD in the preclinical stage.
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Bone marrow-derived mesenchymal stem cells in three-dimensional co-culture attenuate degeneration of nucleus pulposus cells

Xunlin Li, Aimin Wu, Chen Han, Chen Chen, Tangjun Zhou, Kai Zhang, Xiao Yang, Zhiqian Chen, An Qin, Haijun Tian, Jie Zhao,

https://doi.org/10.18632/aging.102390 pp 9167—9187

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Li X, Wu A, Han C, Chen C, Zhou T, Zhang K, Yang X, Chen Z, Qin A, Tian H, Zhao J, . Bone marrow-derived mesenchymal stem cells in three-dimensional co-culture attenuate degeneration of nucleus pulposus cells. . 11:9167-9187. https://doi.org/10.18632/aging.102390

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                TY  - JOUR
                AU  - Li, Xunlin 
                AU  - Wu, Aimin 
                AU  - Han, Chen 
                AU  - Chen, Chen 
                AU  - Zhou, Tangjun 
                AU  - Zhang, Kai 
                AU  - Yang, Xiao 
                AU  - Chen, Zhiqian 
                AU  - Qin, An 
                AU  - Tian, Haijun 
                AU  - Zhao, Jie 
                TI  - Bone marrow-derived mesenchymal stem cells in three-dimensional co-culture attenuate degeneration of nucleus pulposus cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102390
                DO  - 10.18632/aging.102390
                SP  - 9167
                EP  - 9187
                PY  - 
                AB  - Intervertebral disc degeneration (IDD) is an irreversible aging-associated clinical condition of unclear etiology. Mesenchymal stem cells (MSCs) have the potential to delay IDD, but the mechanisms by which MSCs attenuate senescence-related degeneration of nucleus pulposus cells (NPCs) remain uncertain. The present study employed a three-dimensional (3D) co-culture system to explore the influence of MSCs on NPC degeneration induced by TNF-&#x3B1; in rat cells. We found that co-culture with bone marrow-derived MSCs (BMSCs) reduced senescence-associated &#x3B2;-galactosidase expression, increased cell proliferation, decreased matrix metalloproteinase 9, increased Coll-IIa production, and reduced TGF&#x3B2;/NF-&#x3BA;B signaling in senescent NPCs. In addition, expression of zinc metallopeptidase STE24 (ZMPSTE24), whose dysfunction is related to premature cell senescence and aging, was decreased in senescent NPCs but restored upon BMSC co-culture. Accordingly, ZMPSTE24 overexpression in NPCs inhibited the pro-senescence effects of TGF&#x3B2;/NF-&#x3BA;B activation upon TNF-&#x3B1; stimulation, while both CRISPR/Cas9-mediated silencing and pharmacological ZMPSTE24 inhibition prevented those effects. Ex-vivo experiments on NP explants provided supporting evidence for the protective effect of MSCs against NPC senescence and IDD. Although further molecular studies are necessary, our results suggest that MSCs may attenuate or prevent NP fibrosis and restore the viability and functional status of NPCs through upregulation of ZMPSTE24.
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Narrative impairment, white matter damage and CSF biomarkers in the Alzheimer’s disease spectrum

Claudia Drummond, Gabriel Coutinho, Marina Carneiro Monteiro, Naima Assuncao, Alina Teldeschi, Andrea Silveira de Souza, Natalia Oliveira, Ivanei Bramati, Felipe Kenji Sudo, Bart Vanderboght, Carlos Otavio Brandao, Rochele Paz Fonseca, Ricardo de Oliveira-Souza, Jorge Moll, Paulo Mattos, Fernanda Tovar-Moll,

https://doi.org/10.18632/aging.102391 pp 9188—9208

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Drummond C, Coutinho G, Monteiro MC, Assuncao N, Teldeschi A, de Souza AS, Oliveira N, Bramati I, Sudo FK, Vanderboght B, Brandao CO, Fonseca RP, de Oliveira-Souza R, et al, . Narrative impairment, white matter damage and CSF biomarkers in the Alzheimer’s disease spectrum. . 11:9188-9208. https://doi.org/10.18632/aging.102391

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                TY  - JOUR
                AU  - Drummond, Claudia 
                AU  - Coutinho, Gabriel 
                AU  - Monteiro, Marina Carneiro 
                AU  - Assuncao, Naima 
                AU  - Teldeschi, Alina 
                AU  - de Souza, Andrea Silveira 
                AU  - Oliveira, Natalia 
                AU  - Bramati, Ivanei 
                AU  - Sudo, Felipe Kenji 
                AU  - Vanderboght, Bart 
                AU  - Brandao, Carlos Otavio 
                AU  - Fonseca, Rochele Paz 
                AU  - de Oliveira-Souza, Ricardo 
                AU  - Moll, Jorge 
                AU  - Mattos, Paulo 
                AU  - Tovar-Moll, Fernanda 
                TI  - Narrative impairment, white matter damage and CSF biomarkers in the Alzheimer’s disease spectrum
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102391
                DO  - 10.18632/aging.102391
                SP  - 9188
                EP  - 9208
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Drummond, Claudia 
                AU  - Coutinho, Gabriel 
                AU  - Monteiro, Marina Carneiro 
                AU  - Assuncao, Naima 
                AU  - Teldeschi, Alina 
                AU  - de Souza, Andrea Silveira 
                AU  - Oliveira, Natalia 
                AU  - Bramati, Ivanei 
                AU  - Sudo, Felipe Kenji 
                AU  - Vanderboght, Bart 
                AU  - Brandao, Carlos Otavio 
                AU  - Fonseca, Rochele Paz 
                AU  - de Oliveira-Souza, Ricardo 
                AU  - Moll, Jorge 
                AU  - Mattos, Paulo 
                AU  - Tovar-Moll, Fernanda 
                TI  - Narrative impairment, white matter damage and CSF biomarkers in the Alzheimer’s disease spectrum
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102391
                DO  - 10.18632/aging.102391
                SP  - 9188
                EP  - 9208
                PY  - 
                AB  - Background: Narrative discourse (ND) refers to one&#x2019;s ability to verbally reproduce a sequence of temporally and logically-linked events. Impairments in ND may occur in subjects with Amnestic Mild Cognitive Impairment (aMCI) and Alzheimer&#x2019;s Disease (AD), but correlates across this function, neuroimaging and cerebrospinal fluid (CSF) AD biomarkers remain understudied.Objectives: We sought to measure correlates among ND, Diffusion Tensor Imaging (DTI) indexes and AD CSF biomarkers in patients within the AD spectrum.Results: Groups differed in narrative production (NProd) and comprehension. aMCI and AD presented poorer inference abilities than controls. AD subjects were more impaired than controls and aMCI regarding WB (p&lt;0.01). ROIs DTI assessment distinguished the three groups. Mean Diffusivity (MD) in the uncinate, bilateral parahippocampal cingulate and left inferior occipitofrontal fasciculi negatively correlated with NProd. Changes in specific tracts correlated with T-tau/A&#x3B2;1-42 ratio in CSF.Conclusions: AD and aMCI patients presented more ND impairments than controls. Those findings were associated with changes in ventral language-associated and in the inferior parahippocampal pathways. The latest were correlated with biomarkers&#x2019; levels in the CSF.Methods: AD (N=14), aMCI (N=31) and Control (N=39) groups were compared for whole brain (WB) and regions of interest (ROI) DTI parameters, ND and AD CSF biomarkers.
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Overexpression of steroid sulfotransferase genes is associated with worsened prognosis and with immune exclusion in clear cell-renal cell carcinoma

Yuqing Li, Qiang Ding, Zuquan Xiong, Hui Wen, Chenchen Feng,

https://doi.org/10.18632/aging.102392 pp 9209—9219

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Li Y, Ding Q, Xiong Z, Wen H, Feng C, . Overexpression of steroid sulfotransferase genes is associated with worsened prognosis and with immune exclusion in clear cell-renal cell carcinoma. . 11:9209-9219. https://doi.org/10.18632/aging.102392

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                TY  - JOUR
                AU  - Li, Yuqing 
                AU  - Ding, Qiang 
                AU  - Xiong, Zuquan 
                AU  - Wen, Hui 
                AU  - Feng, Chenchen 
                TI  - Overexpression of steroid sulfotransferase genes is associated with worsened prognosis and with immune exclusion in clear cell-renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102392
                DO  - 10.18632/aging.102392
                SP  - 9209
                EP  - 9219
                PY  - 
                AB  - Aim: Steroid sulfotransferase (SULT) plays physiological roles but its role in clear cell-renal cell carcinoma (ccRCC) remains unclear. We therefore investigated genetic alteration of steroid SULT genes in ccRCC.Results: Overexpression of any of SULT genes occurred in ~8% of ccRCC patients. Overexpression of steroid SULT genes was associated with worsened prognosis. Steroid SULT gene-upregulated ccRCC cases showed mutual exclusivity with mutations of VHL, SETD2 and PBRM1, and with focal deletions of 3p and 9p, respectively. Expressions of SULT genes were negatively correlated with that of VHL, SETD2 and PBRM1, respectively. While no cancer-intrinsic pathway was enriched, immune signatures were significantly enriched in SULT gene-overexpressed cases, resulting in significantly fewer infiltration of lymphocytes. Targeting SULT1B1 significantly inhibited growth of ccRCC cells.Conclusion: Steroid SULT genes were associated with worsened prognosis and with immune exclusion in ccRCC.Methods: In silico reproduction of TGGA and GTEx datasets was performed. Data were processed comprehensively using the platforms of cBioPotal, GEPIA, Human Protein Atlas, TIMER, respectively. Functional annotation was analyzed using platforms of NET-GE and GSEA, respectively. In vitro assays were performed for validation.
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Correction for: LAV-BPIFB4 associates with reduced frailty in humans and its transfer prevents frailty progression in old mice

Marco Malavolta, Serena Dato, Francesco Villa, Francesco De Rango, Francesca Iannone, Anna Ferrario, Anna Maciag, Elena Ciaglia, Antonio D'amato, Albino Carrizzo, Andrea Basso, Fiorenza Orlando, Mauro Provinciali, Paolo Madeddu, Giuseppe Passarino, Carmine Vecchione, Giuseppina Rose, Annibale A. Puca,

https://doi.org/10.18632/aging.102398 pp 9220

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Malavolta M, Dato S, Villa F, De Rango F, Iannone F, Ferrario A, Maciag A, Ciaglia E, D'amato A, Carrizzo A, Basso A, Orlando F, Provinciali M, et al, . Correction for: LAV-BPIFB4 associates with reduced frailty in humans and its transfer prevents frailty progression in old mice. . 11:9220-9220. https://doi.org/10.18632/aging.102398

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Provider: 
                TY  - JOUR
                AU  - Malavolta, Marco 
                AU  - Dato, Serena 
                AU  - Villa, Francesco 
                AU  - De Rango, Francesco 
                AU  - Iannone, Francesca 
                AU  - Ferrario, Anna 
                AU  - Maciag, Anna 
                AU  - Ciaglia, Elena 
                AU  - D'amato, Antonio 
                AU  - Carrizzo, Albino 
                AU  - Basso, Andrea 
                AU  - Orlando, Fiorenza 
                AU  - Provinciali, Mauro 
                AU  - Madeddu, Paolo 
                AU  - Passarino, Giuseppe 
                AU  - Vecchione, Carmine 
                AU  - Rose, Giuseppina 
                AU  - Puca, Annibale A. 
                TI  - Correction for: LAV-BPIFB4 associates with reduced frailty in humans and its transfer prevents frailty progression in old mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102398
                DO  - 10.18632/aging.102398
                SP  - 9220
                EP  - 9220
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Malavolta, Marco 
                AU  - Dato, Serena 
                AU  - Villa, Francesco 
                AU  - De Rango, Francesco 
                AU  - Iannone, Francesca 
                AU  - Ferrario, Anna 
                AU  - Maciag, Anna 
                AU  - Ciaglia, Elena 
                AU  - D'amato, Antonio 
                AU  - Carrizzo, Albino 
                AU  - Basso, Andrea 
                AU  - Orlando, Fiorenza 
                AU  - Provinciali, Mauro 
                AU  - Madeddu, Paolo 
                AU  - Passarino, Giuseppe 
                AU  - Vecchione, Carmine 
                AU  - Rose, Giuseppina 
                AU  - Puca, Annibale A. 
                TI  - Correction for: LAV-BPIFB4 associates with reduced frailty in humans and its transfer prevents frailty progression in old mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 20
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102398
                DO  - 10.18632/aging.102398
                SP  - 9220
                EP  - 9220
                PY  - 
                AB  - 
                ER  -

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