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c-Abl contributes to glucose-promoted apoptosis via p53 signaling pathway in podocytes
Yiqiong Ma1, Qian Yang1, Xinghua Chen1
1Division of Nephrology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan 430060, Hubei, China.
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.
Insights
High glucose damages kidney podocytes by increasing c-Abl kinase, which activates the p53 pathway, leading to cell death. Inhibiting c-Abl protects against this high glucose-induced podocyte injury.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Diabetic nephropathy is a leading cause of kidney failure.
- Podocyte injury is a key event in the progression of diabetic nephropathy.
- The role of c-Abl in high glucose-induced podocyte damage is not fully understood.
Purpose of the Study:
- To investigate the involvement of the non-receptor tyrosine kinase c-Abl in high glucose-induced podocyte injury.
- To elucidate the specific signaling pathway through which c-Abl mediates this injury.
Main Methods:
- Mouse models of diabetes and in vitro high glucose exposure of podocytes were used.
- Podocyte apoptosis was assessed using flow cytometry and Hoechst staining.
- c-Abl expression was measured by Western blot and immunofluorescence.
- Co-immunoprecipitation and c-Abl siRNA were employed to study protein interactions and functional effects.
Main Results:
- High glucose exposure significantly increased podocyte apoptosis.
- c-Abl expression was upregulated in podocytes under high glucose conditions.
- Increased c-Abl activity was linked to the activation of the p53 signaling pathway.
- Silencing c-Abl expression ameliorated high glucose-induced podocyte apoptosis and reduced p53 levels.
Conclusions:
- The non-receptor tyrosine kinase c-Abl plays a critical role in high glucose-induced podocyte apoptosis.
- c-Abl mediates podocyte injury through the p53 signaling pathway.
- Targeting c-Abl may represent a therapeutic strategy for diabetic nephropathy.
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