Blockade of TGF-β 1 Signalling Inhibits Cardiac NADPH Oxidase Overactivity in Hypertensive Rats. (3rd June 2012)

• Record Type: Journal Article
• Authors: Miguel-Carrasco, José Luis; Baltanás, Ana; Cebrián, Carolina; Moreno, María U.; López, Begoña; Hermida, Nerea; González, Arantxa; Dotor, Javier; Borrás-Cuesta, Francisco; Díez, Javier; Fortuño, Ana; Zalba, Guillermo
• Other Names: Manea Adrian Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2012(2012)
• Publication Date: 2012-06-03
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2012/726940
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : NADPH oxidases constitute a major source of superoxide anion (⋅ O 2 - ) in hypertension. Several studies suggest an important role of NADPH oxidases in different effects mediated by TGF-β 1. In this study we show that chronic administration of P144, a peptide synthesized from type III TGF-β 1 receptor, significantly reduced the cardiac NADPH oxidase expression and activity as well as in the nitrotyrosine levels observed in control spontaneously hypertensive rats (V-SHR) to levels similar to control normotensive Wistar Kyoto rats. In addition, P144 was also able to reduce the significant increases in the expression of collagen type I protein and mRNA observed in hearts from V-SHR. In addition, positive correlations between collagen expression, NADPH oxidase activity, and nitrotyrosine levels were found in all animals. Finally, TGF-β 1-stimulated Rat-2 exhibited significant increases in NADPH oxidase activity that was inhibited in the presence of P144. It could be concluded that the blockade of TGF-β 1 with P144 inhibited cardiac NADPH oxidase in SHR, thus adding new data to elucidate the involvement of this enzyme in the profibrotic actions of TGF-β 1.