Effects of total replacement of atrial myosin light chain-2 with the ventricular isoform in atrial myocytes of transgenic mice.
Effects of total replacement of atrial myosin light chain-2 with the ventricular isoform in atrial myocytes of transgenic mice.
复制标题
用心室亚型完全替代心房肌球蛋白轻链 2 对转基因小鼠心房肌细胞的影响。
DOI：
10.1161/01.cir.97.15.1508
复制
发表时间：
1998
期刊：
影响因子：
37.8
通讯作者：
Walsh,RA
中科院分区：
文献类型：
--
作者：
Pawloski-Dahm,CM;Song,G;Kirkpatrick,DL;Palermo,J;Gulick,J;Dorn2nd,GW;Robbins,J;Walsh,RA
Background—In contrast to their well-known and critical role in excitation-contraction coupling of vascular smooth muscle, the effects of the myosin light chains on cardiomyocyte mechanics are poorly understood. Accordingly, we designed the present experiment to define the cardiac chamber–specific functional effects of the ventricular isoform of the regulatory myosin light chain (MLC2v).Methods and Results—Postnatal transgenic cardiac-specific overexpression of MLC2v was achieved by use of the α-myosin heavy chain promoter. Enzymatically disaggregated atrial and ventricular mouse myocytes were field-stimulated at multiple frequencies, and mechanical properties and calcium kinetics were studied by use of video edge detection and FURA 2-AM, respectively. MLC2v overexpression resulted in complete replacement of the atrial with the ventricular isoform of the regulatory myosin light chain at the steady-state mRNA and protein levels in the atria of transgenic mice. Mechanical properties of transgenic atrial myocytes were enhanced to the level of ventricular myocytes of control animals in association with modest decreases in the amplitude of the calcium transient.Conclusions—MLC2v modulates chamber-specific contractility by enhanced calcium sensitivity and/or improved cross-bridge cycling of the thin and thick filaments of the cardiomyocyte.
