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Endoglin regulates nitric oxide-dependent vasodilatation

AuthorsJerkic, Mirjana; Rivas-Elena, Juan V.; Prieto, Marta; Carrón, Rosalía; Sanz-Rodríguez, Francisco; Pérez-Barriocanal, Fernando; Rodríguez-Barbero, Alicia; Bernabéu, Carmelo ; López-Novoa, José M.
KeywordsEndoglin haploinsufficiency
Vascular tone
eNOS expression
Issue DateMar-2004
PublisherFederation of American Society of Experimental Biology
CitationFASEB J 18 (3) 609-11 (2004)
AbstractEndoglin is a membrane glycoprotein that plays an important role in cardiovascular development and angiogenesis. We examined the role of endoglin in the control of vascular tone by measuring nitric oxide (NO)-dependent vasodilation in haploinsufficient mice (Eng(+/-)) and their Eng(+/+) littermates. The vasodilatory effect of acetylcholine, bradykinin, and sodium nitroprusside was assessed in anesthetized mice; in isolated, perfused hindlimbs; and in aortic rings. The substantial hypotensive and vasodilatory response induced by acetylcholine and bradykinin in Eng(+/+) was markedly reduced in Eng(+/-) mice. Both kinds of animals had similar responses to sodium nitroprusside, suggesting that the deficient vasodilatory effect is not due to a NO response impairment. Urinary and plasma concentrations of nitrites, a NO metabolite, were lower in Eng(+/-) than in Eng(+/+) mice. The levels of endothelial nitric oxide synthase (eNOS) in kidneys and femoral arteries were about half in Eng(+/-) than in Eng(+/+) mice and were also reduced in primary cultures of aortic endothelial cells from Eng(+/-) compared with those from Eng(+/+) mice. Furthermore, overexpression or suppression of endoglin in cultured cells induced a marked increase or decrease in the protein levels of eNOS, respectively. Thus, our results in vivo and in vitro demonstrate a relationship between endoglin and NO-dependent vasodilation mediated by the regulation of eNOS expression.
Description23 p.-8 fig.
Publisher version (URL)https://doi.org/10.1096/fj.03-0197fje
Appears in Collections:(CIB) Artículos
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