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1 Obstetrics and Gynecology & Physiology, University of Alberta, Edmonton, Alberta, Canada
2 Universidad Industrial de Santander, Bucaramanga, Santander, Colombia; Fundacion Cardiovascular del Oriente, Bucaramanga, Santander, Colombia
* To whom correspondence should be addressed. E-mail: sandra.davidge{at}ualberta.ca.
Abstract-Angiotensin II (AII) has been etiologically linked to vascular disease; however, its role in the alterations of endothelial function that occur in vascular disorders is not completely understood. Matrix metalloproteinases and proinflammatory cytokines have been involved in the pathological remodeling of blood vessels that occurs in vascular disease. In this study we evaluated the effects of AII on TNF
and MMP-2 production in endothelial cells. Human umbilical vein endothelial cells were stimulated with AII (0.1 to 10 mM) for 24 hours, in the presence or absence of antagonists of AT1R and AT2R, and the production and release of TNFa and MMP-2 were assessed. AII increased TNF mRNA, protein expression, and the release of bioactive TNF. Moreover, AII induced MMP-2 release and reduced the secretion of TIMP-2 from endothelial cells. To elucidate whether endogenous TNF could mediate the effects of AII on MMP-2 release, cells were pre-treated with neutralizing antibodies anti-TNF or pentoxifylline (a selective inhibitor of TNF synthesis). TNF inhibition prevented the secretion of MMP-2 induced by AII. Furthermore, AT1R antagonism with candesartan prevented the formation of MMP-2 and TNF, and the reduction of TIMP-2 induced by AII. These results indicate that AII via AT1R modulates the secretion of TNF and MMP-2 from endothelial cells, and that TNF mediates the effects of AII on MMP-2 release.
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