MiR-130a-5p prevents angiotensin II-induced podocyte apoptosis by modulating M-type phospholipase A2 receptor.
OA: closed
Abstract
Podocyte apoptosis is considered as the important element that promotes the development and progress of membranous nephropathy (MN). Unfortunately, the underlying mechanism of podocytes apoptosis in MN remains elusive. We compared the renal expressions of miR-130a-5p and M-type phospholipase A2 receptor (PLA2R) between MN patients (n = 30) and 30 controls by qRT-PCR and western blot, respectively. The podocyte damage model in vitro was established by angiotensin II (Ang II, 100 nmol/L) exposure for 24 h. Interaction between miR-130a-5p and PLA2R was determined using dual-luciferase reporter gene assay. MN mice were induced by intravenous injection of cBSA. In this study, miR-130a-5p expression was significantly decreased both in the renal biopsy specimens from MN patients and podocyte cell line AB8/13 following stimulation of Ang II. Overexpressed miR-130a-5p in AB8/13 cells significantly attenuated the Ang II induced-apoptosis in vitro. In contrast, down-regulated miR-130a-5p induced podocyte apoptosis. PLA2R was identified as the target of miR-130a-5p in AB8/13 cells. And up-regulated or down-regulated PLA2R could obviously attenuate the effect of miR-130a-5p overexpression or knockdown on the apoptosis of AB8/13 cells. Furthermore, it was also observed that overexpressed miR-130a-5p by miR-130a-5p agomir could obviously alleviate renal injury in MN mice. In conclusion, decreased miR-130a-5p was contributed to the pathological mechanism of MN through increasing PLA2R expression, which induced podocyte apoptosis.
My notes (saved in your browser only)
Funding
- funders
- [{'doi': '10.13039/501100001809', 'name': 'National Natural Science Foundation of China', 'awards': ['U1604284']}]
Citation neighborhood (sparse)
Too few in-corpus citations on either side for a chart; here are the lists.
Cites (1)
References (24)
- Peritoneal fluid modifies the microRNA expression profile in endometrial and endometriotic cells from women with endometriosis via crossref
- doi:10.1016/j.kint.2016.03.026 via crossref
- doi:10.1016/j.bbamcr.2009.12.006 via crossref
- doi:10.1038/ki.1994.285 via crossref
- doi:10.1038/35002607 via crossref
- doi:10.1073/pnas.0510928103 via crossref
- doi:10.1016/j.biopha.2015.07.021 via crossref
- doi:10.1056/nejmoa0810457 via crossref
- doi:10.1038/srep06660 via crossref
- doi:10.1186/1471-2164-15-333 via crossref
- doi:10.1152/ajprenal.00569.2016 via crossref
- doi:10.1681/asn.2010090967 via crossref
- doi:10.1016/j.cellsig.2012.11.017 via crossref
- doi:10.1371/journal.pone.0125726 via crossref
- doi:10.1111/jpi.12482 via crossref
- doi:10.1186/s12866-014-0252-0 via crossref
- doi:10.1177/2045893217704206 via crossref
- doi:10.1080/15569527.2017.1355314 via crossref
- doi:10.1096/fj.201700142r via crossref
- doi:10.1093/ndt/gfs439 via crossref
- doi:10.1074/jbc.m113.512780 via crossref
- doi:10.3892/ijmm.2013.1554 via crossref
- doi:10.1681/asn.2004121098 via crossref
- doi:10.1016/j.kint.2017.03.005 via crossref
Source provenance
- crossref
- last seen: 2026-08-12T06:42:44.631928+00:00
- europepmc
- last seen: 2026-08-13T06:15:24.848197+00:00
- unpaywall
- last seen: 2026-08-14T06:25:32.811723+00:00