Decompensation of Pressure-Overload Hypertrophy in Gαq-Overexpressing Mice
作者： Stephen B. Liggett , Richard A. Walsh , Gerald W. Dorn , Yoshihito Sakata , Brian D. Hoit
DOI: 10.1161/01.CIR.97.15.1488
关键词:
摘要: Background—Receptor-mediated activation of myocardial Gq signaling is postulated as a biochemical mechanism transducing pressure-overload hypertrophy. The specific effects on the functional and morphological adaptations to pressure overload are not known. Methods Results—To determine intrinsic myocyte Gαq left ventricular hypertrophic response experimental overload, transgenic mice overexpressing specifically in heart (Gαq-25) nontransgenic siblings underwent microsurgical creation transverse aortic coarctation morphometric, functional, molecular characteristics these pressure-overloaded hearts were compared at increasing times after surgery. Before banding, isolated Gαq-25 myocytes exhibited contractile depression (depressed +dl/dt −dl/dt) showed pattern fetal gene expression similar known mice. Three weeks...
sci-hub.se 参考文章(25)
William Osler, The Principles and Practice of Medicine ,(1892)
K.U. Knowlton, M.C. Michel, M. Itani, H.E. Shubeita, K. Ishihara, J.H. Brown, K.R. Chien, The Alpha 1A-adrenergic Receptor Subtype Mediates Biochemical, Molecular, and Morphologic Features of Cultured Myocardial Cell Hypertrophy Journal of Biological Chemistry. ,vol. 268, pp. 15374- 15380 ,(1993) , 10.1016/S0021-9258(18)82267-0
K U Knowlton, P M McDonough, J H Brown, A N Harris, K R Chien, H E Shubeita, C C Glembotski, Endothelin induction of inositol phospholipid hydrolysis, sarcomere assembly, and cardiac gene expression in ventricular myocytes. A paracrine mechanism for myocardial cell hypertrophy. Journal of Biological Chemistry. ,vol. 265, pp. 20555- 20562 ,(1990) , 10.1016/S0021-9258(17)30538-0
H. A. Rockman, R. S. Ross, A. N. Harris, K. U. Knowlton, M. E. Steinhelper, L. J. Field, J. Ross, K. R. Chien, Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy Proceedings of the National Academy of Sciences of the United States of America. ,vol. 88, pp. 8277- 8281 ,(1991) , 10.1073/PNAS.88.18.8277
Francis G. Dunn, Wille Oigman, Hector O. Ventura, Franz H. Messerli, Isaac Kobrin, Edward D. Frohlich, Enalapril improves systemic and renal hemodynamics and allows regression of left ventricular mass in essential hypertension The American Journal of Cardiology. ,vol. 53, pp. 105- 108 ,(1984) , 10.1016/0002-9149(84)90692-1
Ketty Schwartz, Catherine Chassagne, Kenneth R. Boheler, The molecular biology of heart failure Journal of the American College of Cardiology. ,vol. 22, ,(1993) , 10.1016/0735-1097(93)90459-E
Guillermo E. Garavaglia, Franz H. Messerli, Boris D. Nunez, Roland E. Schmieder, Edward D. Frohlich, Immediate and short-term cardiovascular effects of a new converting enzyme inhibitor (lisinopril) in essential hypertension The American Journal of Cardiology. ,vol. 62, pp. 912- 916 ,(1988) , 10.1016/0002-9149(88)90892-2
Franklin H. Epstein, Arnold M. Katz, Cardiomyopathy of overload. A major determinant of prognosis in congestive heart failure. The New England Journal of Medicine. ,vol. 322, pp. 100- 110 ,(1990) , 10.1056/NEJM199001113220206
John J. Hunter, Nobuaki Tanaka, Howard A. Rockman, John Ross, Kenneth R. Chien, Ventricular Expression of a MLC-2v-ras Fusion Gene Induces Cardiac Hypertrophy and Selective Diastolic Dysfunction in Transgenic Mice Journal of Biological Chemistry. ,vol. 270, pp. 23173- 23178 ,(1995) , 10.1074/JBC.270.39.23173
Arnold M. Katz, The Cardiomyopathy of Overload: An Unnatural Growth Response in the Hypertrophied Heart Annals of Internal Medicine. ,vol. 121, pp. 363- 371 ,(1994) , 10.7326/0003-4819-121-5-199409010-00009