MiR-30a-5p accelerates adipogenesis by negatively regulating Sirtuin 1.

BACKGROUND

Obesity is a chronic metabolic disease characterized by excess fat accumulation. Disordered differentiation of preadipocytes is the leading cause of adipogenesis. Thus, a clarification of the molecular mechanisms that dominate adipocyte differentiation is imperative. MiR-30a-5p is reported to involve in the modulation of multiple cellular processes, including differentiation, whereas, the role of miR-30a-5p in adipocyte differentiation is still unclear.

METHODS

The abundances of miR-30a and Sirtuin 1 (SIRT1) mRNA were detected by RT-qPCR. SIRT1, PPARγ, C/EBPα, and FABP4 protein levels were assessed by western blot (WB). The accumulation of triglyceride (TG) was detected using Triglyceride Content Assay Kit. Cell proliferation activity was evaluated using the MTT assay. Bioinformatics software and the luciferase reporter assay were used to validate the true interaction between miR-30a-5p and SIRT1.

RESULTS

miR-30a-5p expression remains increased during adipocyte differentiation of 3T3-L1 cells. The overexpression of miR-30a-5p enforced adipocyte differentiation, reflected by the enrichment of PPARγ, C/EBPα, FABP4, and triglyceride, as well as the reduction of cell proliferation. SIRT1 was identified as a target of miR-30a-5p, and a supplement of SIRT1 suppressed 3T3-L1 cell differentiation.

CONCLUSION

miR-30a-5p regulated 3T3-L1 cell differentiation by targeting STRT1, supporting the viewpoint that miR-30a-5p might function as a novel therapeutic target for obesity.