C- Abl mediates glucose- induced apoptosis via p53 signaling pathway in podocytes

Abstract

Objective To investigate the role of the non- receptor tyrosine kinase c - Abl in high glucose - induced podocyte injury and its possible signal transduction pathway. Methods Differentiated mouse podocytes were exposed to different glucose concentration conditions in different time slots. Western blotting and immunofluorescence assay were used to measure c-Abl expression and distribution. c-Abl siRNA was transfected to block c-Abl expression. Then podocytes were divided into normal control group(5 mmol/L glucose), high permeability(25 mmol/L mannitol)group, high glucose group and high glucose + c-Abl siRNA group. The podocytes apoptosis was assessed by flow cytometry and Hoechst 33258 staining. The protein expression of c - Abl and p53 was detected by Western blotting. The distribution of c - Abl was observed by immunofluorescence. Co - immunoprecipitation assay was used to evaluate the interaction between c- Abl and p53. Results Compared with normal group, highglucose - induced podocytes had increased apoptosis(P 0.05). Conclusion During the process of high glucose - induced podocytes damage, c - Abl is an apoptosis factor, associated with p53 signaling pathway. Key words: Podocytes; Proto-oncogene protein c-Abl; Apoptosis; Diabetic nephropathy