lncRNA-C920021L13Rik depletion lessened high glucose-induced mesangial cell injury through regulating miR-2861

Abstract

ObjectiveTo explore the biological role of lncRNA-C920021L13Rik (L13Rik for short) in regulating high glucose (HG)-induced injury of glomerular mesangial cell (MC).MethodsThe expressions of L13Rik and miR-2861 in HG-induced glomerular MC were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). And the function of L13Rik on regulating HG-induced MC injury and extracellular matrix (ECM) accumulation was examined by flow cytometry, [35S]-methionine labeling protein synthesis assay and Western blot. A targeted conjugation of miR-2861 with L13Rik was verified by dual-luciferase reporter assay, RNA pull-down and RNA immunoprecipitation (RIP). ResultsL13Rik level spiked markedly while miR-2861 level dropped in HG-treated MCs (P<0.001). Both L13Rik depletion and miR-2861 overexpression effectively lessened HG-induced cell injury and ECM accumulation. L13Rik functioned as a competing endogenous RNA (ceRNA) to sponge miR-2861 for accentuating MC injury.ConclusionL13Rik promotes HG-induced MC injury through regulating miR-2861.

Keywords

• diabetic nephropathy
• mesangial cell
• lncrna-c920021l13rik
• mir-2861