Long non-coding RNA TUG1 alleviates high glucose induced podocyte inflammation, fibrosis and apoptosis in diabetic nephropathy via targeting the miR-27a-3p/E2F3 axis

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD) in developed countries. The long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is associated with mitochondrial function in podocytes in DN. However, the detailed mechanism of TUG1 in DN has not yet been fully elucidated. In this study, we found that the expression levels of TUG1 and E2F transcription factor 3 (E2F3) were downregulated, and microRNA-27a-3p (miR-27a-3p) level was upregulated in DN tissues and HG-treated podocytes. Function analysis indicated that TUG1 overexpression inhibited inflammation, fibrosis and apoptosis in HG-induced podocytes. Rescue experiments demonstrated that miR-27a-3p reversed the suppression effects of TUG1 on apoptosis, fibrosis and inflammation in HG-stimulated podocytes, while E2F3 abrogated the promotion effects of miR-27a-3p on apoptosis, fibrosis and inflammation in HG-induced podocytes. Mechanical analysis revealed that TUG1 regulated E2F3 expression via sponging miR-27a-3p. In conclusion, our findings suggested that TUG1 alleviates high glucose induced inflammation, fibrosis and podocyte apoptosis in diabetic nephropathy via targeting the miR-27a-3p/E2F3 axis, providing a potential therapeutic target for treatment of DN.