Defects in caveolin-1 cause dilated cardiomyopathy and pulmonary hypertension in knockout mice

You Yang Zhao, Yang Liu, Radu Virgil Stan, Lian Fan, Yusu Gu, Nancy Dalton, Po Hsien Chu, Kirk Peterson, John Ross, Kenneth R. Chien*

*此作品的通信作者

研究成果: 期刊稿件文章同行評審

415 引文 斯高帕斯(Scopus)

摘要

Caveolins are important components of caveolae, which have been implicated in vesicular trafficking and signal transduction. To investigate the in vivo significance of Caveolins in mammals, we generated mice deficient in the caveolin-1 (cav-1) gene and have shown that, in the absence of Cav-1, no caveolae structures were observed in several nonmuscle cell types. Although cav-1-/- mice are viable, histological examination and echocardiography identified a spectrum of characteristics of dilated cardiomyopathy in the left ventricular chamber of the cav-1-deficient hearts, including an enlarged ventricular chamber diameter, thin posterior wall, and decreased contractility. These animals also have marked right ventricular hypertrophy, suggesting a chronic increase in pulmonary artery pressure. Direct measurement of pulmonary artery pressure and histological analysis revealed that the cav-1-/- mice exhibit pulmonary hypertension, which may contribute to the right ventricle hypertrophy. In addition, the loss of Cav-1 leads to a dramatic increase in systemic NO levels. Our studies provided in vivo evidence that cav-1 is essential for the control of systemic NO levels and normal cardiopulmonary function.

原文英語
頁(從 - 到)11375-11380
頁數6
期刊Proceedings of the National Academy of Sciences of the United States of America
99
發行號17
DOIs
出版狀態已出版 - 20 08 2002
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