Chronic pressure overload cardiac hypertrophy and failure in guinea pigs: II. Cytoskeletal remodeling

被引:81
作者
Wang, XJ [1 ]
Li, F [1 ]
Campbell, SE [1 ]
Gerdes, AM [1 ]
机构
[1] S Dakota Res Fdn, Cardiovasc Res Inst, Sioux Falls, SD 57105 USA
关键词
cardiac myocytes; cytoskeleton; pressure overload; congestive heart failure; cardiac hypertrophy; microtubules; desmin; titin; myomesin; alpha-actinin;
D O I
10.1006/jmcc.1998.0885
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The cytoskeleton is a major regulator of cell shape. To explore potential mechanisms for maladaptation of cardiac myocyte shape in pressure overload-induced congestive heart failure. the abundance and organization of major intra- and extra-myofibrillar cytoskeleton of cardiac myocytes were examined with western blotting and confocal microscopy in guinea pigs with chronic aortic stenosis. It was found that: (1) the amount and distribution of alpha-actinin and myomesin remained unchanged at both the compensated hypertrophy and the congestive heart failure stages: (2) loss of titin was associated with myocyte lengthening in heart failure; ( 3) desmin protein and filaments in LV myocytes increased progressively with mechanical overload cardiac hypertrophy and subsequent heart failure; (4) a newly developed and validated quantitative confocal microscopic approach disclosed that the microtubule density in isolated LV myocytes increased by 21% at 4 weelrs and by 48% 6 months after aortic constriction; (5) at the heart failure stage, microtubule density in LV myocytes showed a statistically significant inverse correlation to the LV maximum + dP/dt and a direct correlation to LV myocyte lengthening: (6) the increased microtubule density in LV myocytes in this model was not due to an increase in total tubulin; and (7) microtubule density in left atrial and right ventricular myocytes also increased when they underwent hypertrophy secondary to left heart failure. These results suggest that the down-regulation of titin and up-regulation of microtubule and desmin filaments may contribute to myocyte lengthening and malfunction in pressure overload congestive heart failure. (C) 1999 Academic Press.
引用
收藏
页码:319 / 331
页数:13
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