miR-370 promotes high glucose-induced podocyte injuries by inhibiting angiotensin II type 1 receptor-associated protein.

miRNAs expression profiles in podocyte injuries have been reported in different models in vivo and in vitro. In the present study, miR-370 was elevated in high glucose-stimulated podocyte, and the post-transcriptional mechanism of miR-370 was investigated in high glucose-induced podocyte injuries. The gene and protein levels were assayed by RT-qPCR and Western blotting, respectively. Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining was used to evaluate the apoptosis in high glucose-stimulated podocyte. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The results demonstrated that over-activation of miR-370 was verified in high glucose-treated podocytes, while miR-370 repression protected against high glucose-induced apoptosis, cell membrane, and DNA damage in podocytes. We also found that AGTRAP as a direct target of miR-370 served as an opposite effect to miR-370, and overexpression of AGTRAP blocked high glucose-induced podocytes dysfunction. In conclusions, high glucose-induced podocytes damage by activating miR-370 signaling targeted to inhibit the expression of AGTRAP, representing a novel and promising therapeutic target for the treatment of DN.