Effect of miR-29a on apoptosis of renal tubular epithelial cells and its mechanism

Abstract

Objective To investigate the expression of miR-29a in serum of acute kidney injury patients, and whether miR-29a can affect the apoptosis of renal tubular cells by regulating the expressions of phosphatase and tensin homologue deleted on chromosome ten (PTEN). Methods Blood samples were collected from 113 patients with acute kidney injury (AKI) and 110 healthy controls. The expressions of miR-29a in serum were detected by real-fluorescence quantitative polymerase chain reaction (RT-q-PCR). HK-2 cells were cultured in vitro, miR-29a NC or miR-29a mimic was transfected into HK-2 cells, and apoptosis of HK-2 cells was induced by transforming growth factor-β1 (TGF-β1). Flow cytometry was used to investigate the apoptosis of HK-2 cells. Bioinformatics was used to predict potential target genes of miR-29a. Luciferase reporter gene test was used to verify the complementary pairing relationship between miR-29a and PTEN. The expression of PTEN was detected by Western blot. After transfection of plasmids overexpressing PTEN, the apoptosis of HK-2 cells was detected by flow cytometry. Results Compared to the healthy control group, the serum expression of miR-29a was decreased in AKI patients (P<0.05). Flow cytometry results showed that transfection of miR-29a mimic was significantly decreased HK-2 cells apoptosis compared to miR-29 NC group (P<0.05). The Luciferase reporter assay results showed that miR-29a and PTEN had complementary relationship. After transfected with overexpression of PTEN, the HK-2 cells apoptosis rate was significantly increased (P<0.05). Conclusions In the serum of AKI patients, the expression of miR-29a was decreased, overexpression of miR-29a inhibited the apoptosis of renal tubular epithelial cells by inhibiting the expression of PTEN protein. Key words: MicroRNAs/ME; Kidney tubules/CY; Epithelial cells/PA; PTEN phosphohydrolase; Apoptosis