c-Abl contributes to glucose-promoted apoptosis via p53 signaling pathway in podocytes

Diabetes Research and Clinical Practice
Yiqiong MaGuohua Ding

Abstract

To investigate the role of the non-receptor tyrosine kinase c-Abl in high glucose-induced podocyte injury and its possible signal transduction pathway. Sixteen C57BL/6 mice were randomly assigned to a group with diabetes and a normal control group. Subsequently, differentiated mouse podocytes were exposed to high-glucose conditions, and podocyte apoptosis was then assessed by flow cytometry and Hoechst 33258 staining. Western blot and immunofluorescence assay were used to measure c-Abl expression. Co-immunoprecipitation assay was used and c-Abl siRNA was applied to evaluate the interaction between c-Abl and p53. High glucose promotes podocyte apoptosis. The c-Abl expression in podocytes was increased after exposure to high glucose, stimulating the p53 signaling pathway. Conversely, treatment with c-Abl siRNA restored high glucose-promoted podocyte apoptosis and resulted in the reduction of p53 expression. c-Abl contributes to high glucose-induced podocyte apoptosis via p53 signaling pathway.

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Citations

Jul 1, 2017·American Journal of Physiology. Renal Physiology·Yanggang YuanChangying Xing
Jul 20, 2018·Journal of Cellular and Molecular Medicine·Dong-Mei WuYuan-Lin Zheng
Aug 17, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Lu YangYu-Jian Liu

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