JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Add like
Add dislike
Add to saved papers

MiR-21 inhibits autophagy by targeting Rab11a in renal ischemia/reperfusion.

Renal ischemia-reperfusion (I/R) is one of the main causes of the acute kidney injury (AKI) that usually occurs during clinical surgery. Autophagy plays an important role in recovery from acute ischemic kidney injury. MicroRNA-21 (miR-21) was reported to inhibit autophagy in several diseases. However, the molecular mechanism of miR-21 on autophagy during renal I/R is still unclear. For the in vitro study, NRK-52E cells were transfected with miR-21 mimics and subjected to I/R. Results showed that miR-21 mimics inhibited cell viability and induced cell apoptosis in NRK-52E cells. Expression of beclin-1 and LC3-II was induced, and p62 was decreased by I/R. miR-21 mimics inhibited this induction. RT-PCR and western blotting assay showed that miR-21 mimics inhibited the protein level of Rab11a, but not the mRNA level. A luciferase activity assay showed that miR-21 directly targeted Rab11a 3'-UTR. Rab11a overexpression attenuated the effect of miR-21 mimics and I/R on cell viability and cell apoptosis. The expression of beclin-1 and LC3-II was increased, and p62 was decreased by Rab11a overexpression. For the in vivo assay in a rat I/R model, the miR-21 level was increased during renal I/R injury. Pre-treatment with miR-21 inhibitor injection attenuated the renal injury, and enhanced expression of LC3-II and beclin-1. The results showed that miR-21 inhibited autophagy by targeting Rab11a in renal I/R, indicating that Rab11a might be a new medical target for the treatment of renal I/R.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app