Long non-coding RNA ENSMUST00000147869 protects mesangial cells from proliferation and fibrosis induced by diabetic nephropathy.

Abstract

Diabetic nephropathy as the primary cause of end-stage renal disease reveals an increased incidence in patients with kidney disease as the continuous rising of type 2 diabetes. Long non-coding RNAs (lncRNAs) are involved in the development of many diseases including diabetes; however, the role of lncRNAs in diabetic nephropathy is still unclear. In the present study, lncRNA microarray analysis was used to identify abnormally expressed lncRNAs and nearby mRNAs in renal cortical tissues dissected from kidney of db/db and db/m mice. After verifying the data from microarray analysis by quantitative RT-PCR, downregulated ENSMUST00000147869 associated with Cyp4a12a was selected for overexpression in mouse mesangial cells among differentially expressed lncRNAs. Cell Counting Kit-8, Western blotting, and quantitative RT-PCR showed that proliferation and fibrosis indexes were reversed in mesangial cells with ENSMUST00000147869 overexpression. Our data suggested the potential role of ENSMUST00000147869 in proliferation and fibrosis of mesangial cells, which provided a molecular biomarker and therapeutic target for diabetic nephropathy.