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Journal of Diabetes Research
Volume 2018, Article ID 4728645, 11 pages
https://doi.org/10.1155/2018/4728645
Research Article

MicroRNA-22 Promotes Renal Tubulointerstitial Fibrosis by Targeting PTEN and Suppressing Autophagy in Diabetic Nephropathy

1Department of Pathophysiology, Guizhou Medical University, Guiyang, Guizhou 550025, China
2Laboratory of Pathogenesis Research, Drug Prevention and Treatment of Major Diseases, Guizhou Medical University, Guiyang, Guizhou 550025, China

Correspondence should be addressed to Ying Xiao; moc.621@52706002xhxy and Bing Guo; moc.621@sbgniboug

Received 7 September 2017; Revised 3 January 2018; Accepted 14 January 2018; Published 3 April 2018

Academic Editor: Secundino Cigarran

Copyright © 2018 Yingying Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Renal tubulointerstitial fibrosis (TIF) is a major feature of diabetic nephropathy (DN). There is increasing evidence demonstrating that microRNAs act as key players in the regulation of autophagy and are involved in DN. However, the exact link among microRNAs, autophagy, and TIF in DN is largely unknown. In this study, our results showed that TIF was observed in DN rats together with obvious autophagy suppression. Moreover, microRNA-22 (miR-22) was upregulated and associated with reduced expression of its target gene phosphatase and tensin homolog (PTEN) in both the kidneys of DN rats and high glucose-cultured NRK-52E cells. Intriguingly, induction of autophagy by rapamycin antagonized high glucose-induced collagen IV (Col IV) and α-SMA expression. In addition, ectopic expression of miR-22 suppressed autophagic flux and induced the expression of Col IV and α-SMA, whereas the inhibition of endogenous miR-22 effectively relieved high glucose-induced autophagy suppression and the expression of Col IV and α-SMA in NRK-52E cells. Overexpression of PTEN protectively antagonized high glucose- and miR-22-induced autophagy suppression and the expression of Col IV. Therefore, our findings indicated that miR-22 may promote TIF by suppressing autophagy partially via targeting PTEN and represents a novel and promising therapeutic target for DN.