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Am J Physiol Renal Physiol (June 18, 2008). doi:10.1152/ajprenal.90294.2008
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Submitted on May 6, 2008
Revised on May 28, 2008
Accepted on June 12, 2008

Mechanism of Dietary Salt-Mediated Increase in Intravascular Production of TGF-ß1

Wei-Zhong Ying1, Kristal Aaron, and Paul W. Sanders1*

1 University of Alabama at Birmingham

* To whom correspondence should be addressed. E-mail: psanders{at}uab.edu.

Clinical and pre-clinical studies have demonstrated an important effect of arterial pathobiology on the progressive loss of renal function that occurs in chronic kidney disease. Chronic kidney disease, in turn, promotes alterations in vascular function. Amodulating role for dietary salt has been suggested, with the amount of salt intake regulating endothelial cell production of Transforming Growth Factor-{beta}1 (TGF-{beta}1), a fibrogenic growth factor that promotes arteriosclerosis and glomerulosclerosis. The purpose of the present studies was to determine how the interaction between dietary salt intake and vasculature promoted the production of TGF-{beta}1 in rats. Two different vascular tissues - aortic rings and glomeruli - were chosen for study. Dietary salt induced, in a dose-dependent fashion, activation of proline-rich tyrosine kinase-2 (Pyk2) and further identified c-Src as an important binding partner of Pyk2 in these tissues. Use of pharmacological inhibitors and dominant-negative strategies confirmed dietary salt induced complex formation of Pyk2 and c-Src with down stream activation of p38 and p42/44 mitogen-activated protein kinases and generation of TGF-{beta}1. The experiments defined the molecular signaling events that promoted the production of TGF-{beta}1, a key growth factor involved in the vascular response to increased salt intake.




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