Long non-coding RNA L13Rik promotes high glucose-induced mesangial cell hypertrophy and matrix protein expression by regulating miR-2861/CDKN1B axis

Abstract

Glomerular mesangial cell hypertrophy is one of the earliest pathological abnormalities of diabetic nephropathy (DN). A growing literature suggests that lncRNA is involved in the development of DN. However, the function of lncRNA in mesangial cell hypertrophy is still unclear. In the current study, we identified that lncRNA L13Rik was upregulated in DN patients, diabetic rat model and high glucose (HG)-induced mesangial cell. CCK8, Tunel, and western-blot assay were performed to verify the function of silenced L13Rik on the cell growth, apoptosis, and cell hypertrophy in HG-induced mesangial cells. L13Rik knockdown inhibited HG-induced cell proliferation and hypertrophy, while accelerating HG-induced cell apoptosis. Mechanismly, L13Rik regulated mesangial cell hypertrophy by sponging miR-2861. The effect of L13Rik on mesangial hypertrophy was blocked by miR-2861. In addition, L13Rik/miR-2861 promoted mesangial cell hypertrophy by regulating Cyclin-dependent kinase inhibitor 1B (CDKN1B) expression. Taken together, our data showed that L13Rik,as a sponge for miR-2861,regulated protein translation of CDKN1B and led to the hypertrophy of mesangial cell.