MiR-142-3p ameliorates high glucose-induced renal tubular epithelial cell injury by targeting BOD1.

Tubular injury plays a crucial role in the pathogenesis of diabetic nephropathy (DN). It is well known that many microRNAs (miRNAs) exert crucial effects on tubular injury. This study intends to explore the effect of miR-142-3p on the apoptosis and oxidative stress of high glucose (HG)-treated renal tubular epithelial cells (HK-2) and its underlying mechanism. HK-2 cells were exposed to HG to mimic cell injury. MTT assays and flow cytometry analyses were conducted to measure cell viability and cell apoptosis, respectively. RT-qPCR and western blot analyses were carried out to detect RNA and protein levels, respectively. The levels of oxidative stress markers were evaluated by ELISA. The binding between miR-142-3p and biorientation of chromosomes in cell division 1 (BOD1) was validated by a luciferase reporter assay. MiR-142-3p is low-expressed in HG-stimulated HK-2 cells. Functionally, miR-142-3p overexpression attenuates the apoptosis and oxidative stress of HG-stimulated HK-2 cells. Mechanistically, BOD1 was confirmed to be targeted by miR-142-3p in HK-2 cells. Moreover, BOD1 overexpression reversed the suppressive effect of miR-142-3p overexpression on the apoptosis and oxidative stress of HK-2 cells treated with HG. MiR-142-3p ameliorates HG-induced renal tubular epithelial cell injury by targeting BOD1. The finding might provide novel insight into the role of miR-142-3p/BOD1 axis in DN treatment.