c-Abl mediates angiotensin II-induced apoptosis in podocytes

摘要: Angiotensin II (Ang II) has been reported to cause podocyte apoptosis in rats both vivo and vitro studies. However, the underlying mechanisms are poorly understood. In present study, we investigated role of nonreceptor tyrosine kinase c-Abl Ang II-induced apoptosis. Male Sprague–Dawley groups 12 were administered either (400 kg/kg/min) or + STI-571 (50 mg/kg/day) by osmotic minipumps. addition, rats-receiving normal saline served as control. Glomeruli expression was carried out real time PCR, Western blotting immunolabeled, occurrence TUNEL staining transmission electron microscopic analysis. studies, conditionally immortalized mouse podocytes treated with (10−9–10−6 M) presence absence inhibitor, Src-I1, specific siRNA, plasmid alone. Quantification phosphorylation at Y245 Y412 immunofluorescence imaging. The nuclear p53 quantified co-immunoprecipitation Podocyte analysed flow cytometry Hoechst-33342 staining. demonstrated rat kidney cultured vitro. II-receiving displayed enhanced expression. And significantly stimulated podocytes. Furthermore upregulated Y412. also induced an increase protein c-Abl-p53 complexes Down-regulation inhibitor (Src-I1) well siRNA inhibited apoptosis; conversely, podoctyes transfected These findings indicate that may mediates apoptosis, inhibition can protect from injury.