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

被引:10
作者
Ma, Yiqiong [1 ]
Yang, Qian [1 ]
Chen, Xinghua [1 ]
Liang, Wei [1 ]
Ren, Zhilong [1 ]
Ding, Guohua [1 ]
机构
[1] Wuhan Univ, Div Nephrol, Renmin Hosp, 238 Jiefang Rd, Wuhan 430060, Hubei, Peoples R China
基金
美国国家科学基金会;
关键词
Podocytes; High glucose; c-Abl; Apoptosis; II-INDUCED APOPTOSIS; TYROSINE KINASE; ANGIOTENSIN-II; INJURY; CELLS; NEPHROPATHY; RECEPTOR; SURVIVAL; MODEL; BAX;
D O I
10.1016/j.diabres.2015.12.013
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Aim: 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: 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. Results: 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. Conclusion: c-Abl contributes to high glucose-induced podocyte apoptosis via p53 signaling pathway. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:171 / 178
页数:8
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