Highlights
- •Expression of c-Abl in podocytes is up-regulated in the condition of high glucose.
- •c-Abl contributes to high glucose-induced apoptosis of podocytes.
- •Pro-apoptosis factor p53 is involved in c-Abl signaling in the process of podocytes apoptosis.
Abstract
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.
Keywords
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Article info
Publication history
Published online: January 13, 2016
Accepted:
December 26,
2015
Received in revised form:
November 5,
2015
Received:
August 17,
2015
Identification
Copyright
© 2016 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.