Background
Diabetic nephropathy (DN), as a complication of diabetes, is a leading cause of mortality in diabetic patients. It has been reported that lncRNA PVT1 (PVT1) could accelerate the progression of DN by promoting ECM accumulation and increasing the expression of fibronectin 1 (FN1). However, the underlying mechanism of PVT1 on DN remains unknown.
Conclusion
PVT1 inhibits viability, oxidative stress, fibrosis, and inflammation in DN via miR-325-3p/Snail1 axis.
Methods
To study the effect of PVT1 on DN, mice were injected 50 mg/kg STZ to build the DN models. Mesangial cells (MCs) were induced by high glucose as in vitro model of DN. The expression level of PVT1, miR-325-3 and Snail1 was assessed by qRT-PCR and Western blot. Luciferase reporter assay, RNA pull-down and RIP were used to explore the interaction among PVT1, miR-325-3 and Snail1.
Results
In in vivo and in vitro DN models, the expression of PVT1 was upregulated. High glucose (HG) induced cell viability, oxidative stress, fibrosis and inflammation in MCs, which were reversed in the PVT1-KD MCs. The level of miR-325-3p was also increased in in vivo and in vitro experiments. Additionally, PVT1 can directly bind to miR-325-3p. Finally, Snail1 was a direct target of miR-325-3p.