Bradykinin induces tubulin phosphorylation and nuclear translocation of MAP kinase in mesangial cells

The American Journal of Physiology
A A JaffaR K Mayfield

Abstract

Glomerular hypertension and glomerular hypertrophy act early and synergistically to promote glomerular injury in diabetes. We have previously shown that increased renal kinin production contributes to the glomerular hemodynamic abnormalities associated with diabetes. Glomerulosclerosis, characterized by mesangial cell proliferation and matrix expansion, is the final pathway leading to renal failure. The signal(s) initiating mesangial cell proliferation is ill defined. In the present study, we utilized immunofluorescence, immunoprecipitation, and immunoblotting techniques to identify substrates that are tyrosine phosphorylated in response to bradykinin action in mesangial cells. Immunofluorescence microscopy of mesangial cells stained with anti-phosphotyrosine (anti-PY) antibodies following bradykinin treatment (10(-9)-10(-6) M) revealed a dose-dependent increase in the labeling of cytoplasmic and nuclear proteins. Immunoprecipitation with anti-PY, followed by immunoblot revealed bradykinin-induced tyrosyl phosphorylation of tubulin and mitogen-activated protein kinase (MAPK). Confocal microscopy of mesangial cells stained for MAPK indicated that bradykinin stimulation resulted in translocation of MAPK from the cytoplasm to the ...Continue Reading

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Citations

Sep 21, 2000·American Journal of Physiology. Renal Physiology·W TianD M Cohen
Feb 5, 2005·American Journal of Physiology. Renal Physiology·Yan TanAyad A Jaffa
Feb 27, 2003·The Journal of Pharmacology and Experimental Therapeutics·Yurii V MukhinMaria N Garnovskaya
Oct 9, 2015·American Journal of Physiology. Renal Physiology·J Abou MsallemAyad A Jaffa
Oct 22, 2008·Biochemical Pharmacology·Inga I KramarenkoMaria N Garnovskaya

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