Retraction statement: ‘Urotensin II inhibits autophagy in renal tubular epithelial cells and induces extracellular matrix production in early diabetic mice’ by Guan‐Jong Chen, Fei Wu, Xin‐Xin Pang, Ai‐Hua Zhang, Jun‐Bao Shi, Min Lu and Chao‐Shu Tang

Autor: Chen GJ; Department of Nephrology, Peking University Third Hospital, Beijing, China., Wu F; Department of Nephrology, Peking University Third Hospital, Beijing, China., Pang XX; Department of Nephrology, Peking University Third Hospital, Beijing, China., Zhang AH; Department of Nephrology, Peking University Third Hospital, Beijing, China., Shi JB; Department of Nephrology, Peking University Third Hospital, Beijing, China., Lu M; Department of Pathology, Peking University Health Science Center, Beijing, China., Tang CS; Department of Pathology and Physiology, Peking University Health Science Center, Beijing, China.
Jazyk: angličtina
Zdroj: Journal of diabetes investigation [J Diabetes Investig] 2017 Jul; Vol. 8 (4), pp. 629. Date of Electronic Publication: 2016 Jul 26.
DOI: 10.1111/jdi.12557
Abstrakt: Aims/introduction: Urotensin II (UII) and autophagy have been considered as important components in the pathogenesis of diabetic nephropathy. The present study explores whether UII can regulate autophagy in the kidney, and its effect in diabetes.
Materials and Methods: Immunohistochemistry and western blot were carried out on the kidney tissues of diabetic UII receptor (UT) gene knockout mice, wild-type diabetic mice and normal control mice. For the in vitro experiment, HK-2 cells were treated with UII (10 -7 mol/L) in the presence or absence of UT antagonist, SB-657510, (10 -6 mol/L) or autophagy inducer, rapamycin (10 -3 mol/L), for 12 h. Markers for autophagy (LC3-II, p62/SQSTM1) and extracellular matrix (fibronectin, collagen IV) were analyzed.
Results: In diabetic UT knockout mice, expression of LC3-II is increased and p62 was reduced in comparison with that of the normal diabetic mice. Fibronectin and collagen IV were downregulated in diabetic UT knockout mice when compared with that of the normal diabetic mice. For the in vitro cell experiment, UII was shown to inhibit expression LC3-II and increase expression of p62 in comparison with that of the normal control. Treatment with SB-657510 can block UII-induced downregulation of LC3-II and upregulation of p62 while inhibiting UII-induced upregulation of fibronectin and collagen IV. Adding autophagy inducer, rapamycin, also inhibited UII-induced upregulation of fibronectin and collagen IV.
Conclusions: The present study is the first to show that UII can downregulate autophagy in the kidney while accompanying the increased production of extracellular matrix in early diabetes. Our in vitro study also showed that upregulation of autophagy can decrease UII-induced production of extracellular matrix in HK-2 cells.
(© 2016 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd.)
Databáze: MEDLINE
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