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Research Article| Volume 113, P171-178, March 2016

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

Published:January 13, 2016DOI:https://doi.org/10.1016/j.diabres.2015.12.013

      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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