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7. CERS6-derived ceramides aggravate kidney fibrosis by inhibiting PINK1-mediated mitophagy in diabetic kidney disease

Author

Wang, Xiangyu, primary, Song, Minkai, additional, Li, Xiaomin, additional, Su, Cailin, additional, Yang, Yanlin, additional, Wang, Kai, additional, Liu, Cuiting, additional, Zheng, Zongji, additional, Jia, Yijie, additional, Ren, Shijing, additional, Dong, Wenhui, additional, Chen, Jiaqi, additional, Wang, Ting, additional, Liu, Lerong, additional, Guan, Meiping, additional, Zhang, Chao, additional, and Xue, Yaoming, additional

Published
2023
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12. The HDAC2/SP1/miR-205 feedback loop contributes to tubular epithelial cell extracellular matrix production in diabetic kidney disease

Author

Zheng, Zongji, primary, Zhang, Shuting, additional, Chen, Jiaqi, additional, Zou, Meina, additional, Yang, Yanlin, additional, Lu, Wen, additional, Ren, Shijing, additional, Wang, Xiangyu, additional, Dong, Wenhui, additional, Zhang, Zikun, additional, Wang, Ling, additional, Guan, Meiping, additional, Cheing, Gladys L.Y., additional, Xue, Yaoming, additional, and Jia, Yijie, additional

Published
2022
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14. High-Salt Attenuates the Efficacy of Dapagliflozin in Tubular Protection by Impairing Fatty Acid Metabolism in Diabetic Kidney Disease

Author

Zou, Meina, primary, Chen, Yanrong, additional, Zheng, Zongji, additional, Sheng, Shuyue, additional, Jia, Yijie, additional, Wang, Xiangyu, additional, Ren, Shijing, additional, Yang, Yanling, additional, Li, Xiaomin, additional, Dong, Wenhui, additional, Guan, Meiping, additional, Zhang, Qian, additional, and Xue, Yaoming, additional

Published
2021
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15. MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice

Author

Fang, Shu, Feng, Jie, Zhang, Hongbin, Li, Ping, Zhang, Yudan, Zeng, Yanmei, Cai, Yingying, Lin, Xiaochun, Xue, Yaoming, Guan, Meiping, Fang, Shu, Feng, Jie, Zhang, Hongbin, Li, Ping, Zhang, Yudan, Zeng, Yanmei, Cai, Yingying, Lin, Xiaochun, Xue, Yaoming, and Guan, Meiping

Abstract

MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver of db/db diabetic mice and explore the potential mechanisms. Diabetic mice (db/db) and control mice (db/m) were randomly divided into four groups. After overexpression of miR-455 in the liver of db/db mice, the triglycerides level in both serum and liver decreased, the lipid deposit in liver was improved, the expression of fatty acid synthase, stearoyl-CoA desaturase 1, sterol regulatory element binding protein 1c (SREBP-1c) and acetyl-CoA carboxylase (ACCα) was also significantly down-regulated. TargetScan indicated that suppressor of cytokine signalling 3 (SOCS3) is predicated to target miR-455 and the protein of SOCS3 in the liver of db/db mice after intervention was significantly decreased. The dual luciferase reporter assay showed that SOCS3 was target gene of miR-455. In vitro, in Palmitate (PA)-stimulated human normal liver (LO2) cells, transfected miR-455 mimic could significantly inhibit the expression of SOCS3, while transfected miR-455 inhibitor could up-regulate the expression of SOCS3. Transfecting LO2 cells with siRNA of SOCS3 could significantly down-regulate the protein expression of SREBP-1c and ACCα. Our study showed that overexpression of miR-455 in the liver could improve lipid metabolism in diabetic mice by down-regulating its target gene SOCS3.

Published
2020

16. Transplantation of brown adipose tissue up-regulates miR-99a to ameliorate liver metabolic disorders in diabetic mice by targeting NOX4

Author

Li, Ping, Fan, Cunxia, Cai, Yingying, Fang, Shu, Zeng, Yanmei, Zhang, Yudan, Lin, Xiaochun, Zhang, Hongbin, Xue, Yaoming, Guan, Meiping, Li, Ping, Fan, Cunxia, Cai, Yingying, Fang, Shu, Zeng, Yanmei, Zhang, Yudan, Lin, Xiaochun, Zhang, Hongbin, Xue, Yaoming, and Guan, Meiping

Abstract

Nonalcoholic fatty liver disease (NAFLD), main cause of liver damage, is inextricably linked to diabetes. However, there is no specific means to improve the pathology of fatty liver in diabetic patients. Brown adipose tissue (BAT) is an important endocrine organ that secretes adipokines and microRNAs (miRNAs) involved in systemic metabolic regulation. To investigate the effects of BAT transplantation on liver lipid metabolism in diabetic mice, we transplanted BAT from male donor mice into diabetic mice induced by streptozotocin (STZ) combined with high-fat diet (HFD). At 10 weeks after transplantation, BAT transplantation significantly decreased the blood glucose and lipid, downregulated FAS, CD36, Scd1, ACC alpha, NOX2, NOX4, TGF-beta 1, FN and COL-1, up-regulated Nrf2, reversed the pathological changes of liver and increased the circulating miR-99a in diabetic mice. To verify whether circulating miR-99a improves oxidative stress by targeting inhibition of NOX4, we used 0.4mM palmitic acid (PA) to treat the LO2 cells. The expression of NOX4 protein was significantly decreased after transfection with miR-99a mimic, and increased after transfection with miR-99a inhibitor. Luciferase reporter assay confirmed that miR-99a could target NOX4 mRNA. These findings clarify the role of miR-99a and NOX4 in liver beneficial effect of BAT transplantation in diabetic mice.

Published
2020

17. Exendin-4 Improves Diabetic Kidney Disease in C57BL/6 Mice Independent of Brown Adipose Tissue Activation

Author

Fang, Shu, Cai, Yingying, Lyu, Fuping, Zhang, Hongbin, Wu, Chunyan, Zeng, Yanmei, Fan, Cunxia, Zou, Shaozhou, Zhang, Yudan, Li, Ping, Wang, Ling, Xue, Yaoming, Guan, Meiping, Fang, Shu, Cai, Yingying, Lyu, Fuping, Zhang, Hongbin, Wu, Chunyan, Zeng, Yanmei, Fan, Cunxia, Zou, Shaozhou, Zhang, Yudan, Li, Ping, Wang, Ling, Xue, Yaoming, and Guan, Meiping

Abstract

Background. The role of exendin-4 in brown adipose tissue (BAT) activation was not very clear. This study is to verify the role of BAT involved in renal benefits of exendin-4 in diabetes mellitus (DM). Methods. In vivo, C57BL/6 mice were randomly divided into nondiabetic (control) and diabetic groups (DM). The diabetic mice were randomized into a control group (DM-Con), BAT-excision group (DM+Exc), exendin-4-treated group (DM+E4), and BAT-excision plus exendin-4-treated group (DM+Exc+E4). The weight, blood glucose and lipids, 24 h urine albumin and 8-OH-dG, and renal fibrosis were analyzed. In vitro, we investigated the role of exendin-4 in the differentiation process of 3T3-L1 and brown preadipocytes and its effect on the rat mesangial cells induced by oleate. Results. The expressions of UCP-1, PGC-1 alpha, ATGL, and CD36 in BAT of DM mice were all downregulated, which could be upregulated by exendin-4 treatment with significant effects on ATGL and CD36. BAT-excision exacerbated high blood glucose (BG) with no significant effect on the serum lipid level. Exendin-4 significantly lowered the level of serum triglycerides (TG) and low-density lipoprotein- (LDL-) c, 24 h urine albumin, and 8-OH-dG; improved renal fibrosis and lipid accumulation; and activated renal AMP-activated protein kinase (AMPK) in diabetic mice regardless of BAT excision. In vitro, there was no significant effect of exendin-4 on brown or white adipogenesis. However, exendin-4 could improve lipid accumulation and myofibroblast-like phenotype transition of mesangial cells induced by oleate via activating the AMPK pathway. Conclusions. Exendin-4 could decrease the renal lipid deposit and improve diabetic nephropathy via activating the renal AMPK pathway independent of BAT activation.

Published
2020

18. Inhibiting Rab27a in renal tubular epithelial cells attenuates the inflammation of diabetic kidney disease through the miR-26a-5p/CHAC1/NF-kB pathway

Author

Li, Shuangshuang, primary, Jia, Yijie, additional, Xue, Meng, additional, Hu, Fang, additional, Zheng, Zongji, additional, Zhang, Shuting, additional, Ren, Shijing, additional, Yang, Yanlin, additional, Si, Zekun, additional, Wang, Ling, additional, Guan, Meiping, additional, and Xue, Yaoming, additional

Published
2020
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21. 26-LB: Exenatide and Renal Outcomes in Patients with Type 2 Diabetes and Diabetic Kidney Disease: A Multicenter, Randomized, Parallel Study

Author

WANG, XIANGYU, primary, ZHANG, QIAN, additional, GUAN, MEIPING, additional, SHENG, SHUYUE, additional, MO, WEI, additional, ZOU, MENGCHEN, additional, LI, JIMIN, additional, BI, JIANLU, additional, TANG, XIANYU, additional, HE, JIALI, additional, XU, GUGEN, additional, LI, PING, additional, ZHANG, HUIJIE, additional, and XUE, YAOMING, additional

Published
2020
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22. Exenatide and renal outcomes in patients with type 2 diabetes and diabetic kidney disease: a multi-center, randomized, parallel study

Author

Wang, Xiangyu, primary, Zhang, Qian, additional, Guan, Meiping, additional, Sheng, Shuyue, additional, Mo, Wei, additional, Zou, Mengchen, additional, Li, Jimin, additional, Bi, Jianlu, additional, Tang, Xianyu, additional, He, Jiali, additional, Xu, Gugen, additional, Li, Ping, additional, Zhang, Huijie, additional, and Xue, Yaoming, additional

Published
2020
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25. Exenatide and Renal Outcomes in Patients with Type 2 Diabetes and Diabetic Kidney Disease

Author

Wang, Xiangyu, primary, Zhang, Huijie, additional, Zhang, Qian, additional, Guan, Meiping, additional, Sheng, Shuyue, additional, Mo, Wei, additional, Zou, Mengchen, additional, Li, Jimin, additional, Bi, Jianlu, additional, Tang, Xianyu, additional, Zeng, Huiyan, additional, He, Jiali, additional, Xu, Gugen, additional, Li, Ping, additional, and Xue, Yaoming, additional

Published
2020
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26. Increased oxidative stress, inflammation and fibrosis in perirenal adipose tissue of patients with cortisol-producing adenoma

Author

Wu, Chunyan, Zhang, Huijian, Zhang, Jiajun, Zhang, Hongbin, Zeng, Yanmei, Fang, Shu, Li, Ping, Zhang, Yudan, Lin, Xiaochun, Wang, Ling, Xue, Yaoming, Guan, Meiping, Wu, Chunyan, Zhang, Huijian, Zhang, Jiajun, Zhang, Hongbin, Zeng, Yanmei, Fang, Shu, Li, Ping, Zhang, Yudan, Lin, Xiaochun, Wang, Ling, Xue, Yaoming, and Guan, Meiping

Abstract

Although much is known about that corticosteroids affect the functions of adipose tissues, little genetic information is available for perirenal adipose tissue (peri-N) from patients with cortisol-producing adenoma (CPA). We conducted microarray analysis of peri-N from patients with CPA by using an Affymetrix human U133 plus 2.0 array. We also analysed the inflammation, fibrosis and oxidative stress in vitro. Compared with normotension (NT) group, CPA group has significantly higher protein levels of TNF alpha, IL-6, fibronectin (FN) and collagen I (COLI). The protein level of NADPH oxidase 4 (Nox4) significantly increased, while nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) levels were significantly reduced in the CPA group. Dexamethasone markedly induced fibrosis and adipogenesis-related gene expression in predifferentiated stromal vascular fraction (SVF) cells, 3T3-L1 preadipocytes and brown preadipocytes. Chronic exposure to endogenous glucocorticoids due to CPA increases peri-N oxidative stress, inflammation and fibrosis, which may contribute to the metabolic disturbances associated with hypercortisolism in these patients.

Published
2019

38. MiR‐4756 promotes albumin‐induced renal tubular epithelial cell epithelial‐to‐mesenchymal transition and endoplasmic reticulum stress via targeting Sestrin2.

Author

Jia, Yijie, Zheng, Zongji, Yang, Yanlin, Zou, Meina, Li, Jimin, Wang, Ling, Guan, Meiping, and Xue, Yaoming

Subjects
DIABETIC nephropathies, MICRORNA, EPITHELIAL cells, ENDOPLASMIC reticulum, TYPE 2 diabetes
Abstract

Accumulating evidence indicates that proteinuria promotes the progression of diabetic kidney disease (DKD) and induces renal epithelial tubular cell epithelial‐to‐mesenchymal transition (EMT) and endoplasmic reticulum (ER) stress, but the mechanism remains unclear. In our previous research, we found that miR‐4756 levels were increased in the urinary extracellular vesicles of type 2 diabetes mellitus patients with macroalbuminuria. In a preliminary study, we found that miR‐4756 may be derived from renal tubular epithelial cells, but its role has not been elucidated. Albumin stimulation significantly increased miR‐4756 levels in HK‐2 cells. In addition, an miR‐4756 mimic accelerated albumin‐stimulated HK‐2 cell EMT and ER stress, and an miR‐4756 inhibitor suppressed these events. We then found that miR‐4756 targeted the 3′‐untranslated region (UTR) of Sestrin2 and directly suppressed Sestrin2 expression. Furthermore, the induction of EMT and ER stress by the overexpression of miR‐4756 was abolished by Sestrin2 overexpression. Moreover, the overexpression of miR‐4756 increased ERK1/2 activation and decreased 5′ monophosphate‐activated protein kinase activation. Thus, our study provides evidence that miR‐4756 accelerates the process of DKD through Sestrin2, suggesting that targeting miR‐4756 may be a novel strategy for DKD treatment. MiR‐4756 exerts its effect by targeting Sestrin2, which inhibits renal epithelial‐to‐mesenchymal transition and endoplasmic reticulum stress during diabetic kidney disease (DKD). MiR‐4756 content was also increased in urinary extracellular vesicles of DKD patients and extracellular vesicles derived from human serum albumin‐treated HK‐2 cells, which indicated that miR‐4756 in urinary extracellular vesicles may reflect the pathophysiological changes during DKD. [ABSTRACT FROM AUTHOR]

Published
2019
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39. The coordinated roles of miR-26a and miR-30c in regulating TGFβ1-induced epithelial-to-mesenchymal transition in diabetic nephropathy

Author

Zheng, Zongji, Guan, Meiping, Jia, Yijie, Wang, Dan, Pang, Ruoyu, Lv, Fuping, Xiao, Zhizhou, Wang, Ling, Zhang, Hongbin, Xue, Yaoming, Zheng, Zongji, Guan, Meiping, Jia, Yijie, Wang, Dan, Pang, Ruoyu, Lv, Fuping, Xiao, Zhizhou, Wang, Ling, Zhang, Hongbin, and Xue, Yaoming

Abstract

MicroRNAs (miRNAs) play vital roles in the development of diabetic nephropathy. Here, we compared the protective efficacies of miR-26a and miR-30c in renal tubular epithelial cells (NRK-52E) and determined whether they demonstrated additive effects in the attenuation of renal fibrosis. TGFβ1 suppressed miR-26a and miR-30c expression but up-regulated pro-fibrotic markers in NRK-52E cells, and these changes were also found in the kidney cortex of 40-week-old diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats. Bioinformatic analyses and luciferase assays further demonstrated that both miR-26a and miR-30c targeted connective tissue growth factor (CTGF); additionally, Snail family zinc finger 1 (Snail1), a potent epithelial-to-mesenchymal transition (EMT) inducer, was targeted by miR-30c. Overexpression of miR-26a and miR-30c coordinately decreased CTGF protein levels and subsequently ameliorated TGFβ1-induced EMT in NRK-52E cells. Co-silencing of miR-26a and miR-30c exhibited the opposite effect. Moreover, miR-26a and miR-30c co-silenced CTGF to decrease ERK1/2 and p38 MAPK activation. Furthermore, miR-26a was up-regulated in urinary extracellular vesicles of diabetic nephropathy patients. Our study provides evidence for the cooperative roles of miR-26a and miR-30c in the pathogenesis of diabetic nephropathy, and the co-targeting of miR-26a and miR-30c could provide a new direction for diabetic nephropathy treatment.

Published
2016

43. Micro RNA ‐455 regulates brown adipogenesis via a novel HIF 1an‐ AMPK ‐ PGC 1α signaling network

Author

Zhang, Hongbin, primary, Guan, Meiping, additional, Townsend, Kristy L, additional, Huang, Tian Lian, additional, An, Ding, additional, Yan, Xu, additional, Xue, Ruidan, additional, Schulz, Tim J, additional, Winnay, Jonathon, additional, Mori, Marcelo, additional, Hirshman, Michael F, additional, Kristiansen, Karsten, additional, Tsang, John S, additional, White, Andrew P, additional, Cypess, Aaron M, additional, Goodyear, Laurie J, additional, and Tseng, Yu‐Hua, additional

Published
2015
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50. miRNAs in Urine Extracellular Vesicles as Predictors of Early-Stage Diabetic Nephropathy.

Author

Jia, Yijie, Guan, Meiping, Zheng, Zongji, Zhang, Qian, Tang, Chuan, Xu, Wenwei, Xiao, Zhizhou, Wang, Ling, and Xue, Yaoming

Subjects
*DIABETIC nephropathies, *MICRORNA, *VESICLES (Cytology), *KIDNEY tubules, *EPITHELIAL cells, *BIOMARKERS
Abstract

Background. miR-192, miR-194, and miR-215 are enriched in the kidney and play roles in the pathogenesis of diabetic nephropathy (DN). Extracellular vesicles (EVs) can be detected in body fluids and may serve as disease biomarkers. Methods. Eighty type 2 diabetes patients with normoalbuminuria (n=30), microalbuminuria (n=30), or macroalbuminuria (n=20), as well as 10 healthy controls, were enrolled in this study. Real-time PCR was used to evaluate urinary EV miRNAs expression. Results. The miR-192 levels were significantly higher than the miR-194 and miR-215 levels in urine EVs and all three miRNAs were significantly increased in the microalbuminuric group compared with the normoalbuminuric and control subjects but were decreased in the macroalbuminuric group. In patients with normoalbuminuria and microalbuminuria, miR-192 was positively correlated with albuminuria (r=0.357, P=0.005) levels and transforming growth factor- (TGF-) β1 (r=0.356, P=0.005) expression. Receiver operating characteristic (ROC) curve analysis revealed that miR-192 was better than miR-194 and miR-215 in discriminating the normoalbuminuric group from the microalbuminuric group. Exposure of human renal tubular epithelial cells to high glucose increased the expression of both miRNAs in cellular supernatant EVs, indicating a potential source. Conclusion. These results suggest the potential use of urinary EV miR-192 as a biomarker of the early stage of DN. [ABSTRACT FROM AUTHOR]

Published
2016
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