Differences in the spatial distribution of actin in the left and right ventricles of functioning rabbit hearts

J. Nagwekar , D. Duggal , R. Rich , R. Fudala , I. Gryczynski , S. Raut , Z. Gryczynski , J. Borejdo
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引用次数: 2

Abstract

We examined the effect of the differences in spatial arrangement of actin in contracting muscles from the left (LV) and right (RV) ventricles of rabbit heart. Spatial arrangement is a fundamental property of muscle because it reflects the interaction of individual actin molecules with myosin cross-bridges. Macroscopic parameters of contraction, such as maximum tension, speed of shortening or ATPase activity, are unlikely to reveal differences between the ventricles because they are made on whole organs containing trillions of actin and myosin molecules. Averaging the data collected from such a large assembly is likely to conceal small differences. To eliminate complications arising from the differences in the basic myocardial architecture and fiber structures of the ventricles, and to ensure that the molecular crowding influences contraction in the same way as under the in-vivo conditions, we collected data from isolated myofibrils ex-vivo. Control anisotropy experiments revealed that the orientation of actin reflected the orientation of myosin cross-bridges. The results showed that the changes in the distribution of actin induced by the interaction of actin filaments with myosin heads were demonstrated only in LVs, not in RVs. This suggests that both ventricles interact differently with myosin cross-bridges. We think that the stress induced in the thin filaments of LV causes loosening of bonds between actin monomers which leads to greater mobility of actin monomers.

功能兔左、右心室肌动蛋白空间分布的差异
我们研究了兔左心室和右心室收缩肌中肌动蛋白空间排列差异的影响。空间排列是肌肉的基本特性,因为它反映了单个肌动蛋白分子与肌凝蛋白交叉桥的相互作用。收缩的宏观参数,如最大张力、缩短速度或atp酶活性,不太可能揭示心室之间的差异,因为它们是在包含数万亿肌动蛋白和肌球蛋白分子的整个器官上形成的。对从这么大的集合中收集的数据进行平均可能会掩盖微小的差异。为了消除心肌基本结构和心室纤维结构差异引起的并发症,并确保分子拥挤影响收缩的方式与在体条件下相同,我们从离体分离的肌原纤维中收集数据。对照各向异性实验表明,肌动蛋白的取向反映了肌凝蛋白桥的取向。结果表明,肌动蛋白丝与肌凝蛋白头相互作用引起的肌动蛋白分布的变化仅在lv中出现,而在rv中没有。这表明两个心室与肌凝蛋白交叉桥的相互作用不同。我们认为,在LV细丝中诱导的应力导致肌动蛋白单体之间的键松动,从而导致肌动蛋白单体的流动性增强。
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