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人类心脏左、右心室肌球蛋白动力学及杠杆臂空间分布无差异。

No Difference in Myosin Kinetics and Spatial Distribution of the Lever Arm in the Left and Right Ventricles of Human Hearts.

作者信息

Duggal Divya, Requena S, Nagwekar Janhavi, Raut Sangram, Rich Ryan, Das Hriday, Patel Vipul, Gryczynski Ignacy, Fudala Rafal, Gryczynski Zygmunt, Blair Cheavar, Campbell Kenneth S, Borejdo Julian

机构信息

Department of Cell Biology and Center for Commercialization of Fluorescence Technologies, University of North Texas, Health Science Center, Fort Worth, TX, United States.

Department of Physics and Astronomy, Texas Christian University, Fort Worth, TX, United States.

出版信息

Front Physiol. 2017 Oct 13;8:732. doi: 10.3389/fphys.2017.00732. eCollection 2017.

DOI:10.3389/fphys.2017.00732
PMID:29081749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5645524/
Abstract

The systemic circulation offers larger resistance to the blood flow than the pulmonary system. Consequently, the left ventricle (LV) must pump blood with more force than the right ventricle (RV). The question arises whether the stronger pumping action of the LV is due to a more efficient action of left ventricular myosin, or whether it is due to the morphological differences between ventricles. Such a question cannot be answered by studying the entire ventricles or myocytes because any observed differences would be wiped out by averaging the information obtained from trillions of myosin molecules present in a ventricle or myocyte. We therefore searched for the differences between single myosin molecules of the LV and RV of failing hearts . We show that the parameters that define the mechanical characteristics of working myosin (kinetic rates and the distribution of spatial orientation of myosin lever arm) were the same in both ventricles. These results suggest that there is no difference in the way myosin interacts with thin filaments in myocytes of failing hearts, and suggests that the difference in pumping efficiencies are caused by interactions between muscle proteins other than myosin or that they are purely morphological.

摘要

体循环对血流的阻力比肺循环更大。因此,左心室(LV)必须比右心室(RV)更用力地泵血。问题在于,左心室更强的泵血作用是由于左心室肌球蛋白的作用更高效,还是由于心室之间的形态差异。通过研究整个心室或心肌细胞无法回答这个问题,因为任何观察到的差异都会被来自心室或心肌细胞中数万亿个肌球蛋白分子的平均信息所掩盖。因此,我们研究了衰竭心脏左心室和右心室单个肌球蛋白分子之间的差异。我们发现,定义工作肌球蛋白力学特性的参数(动力学速率和肌球蛋白杠杆臂空间取向分布)在两个心室中是相同的。这些结果表明,在衰竭心脏的心肌细胞中,肌球蛋白与细肌丝相互作用的方式没有差异,这表明泵血效率的差异是由肌球蛋白以外的肌肉蛋白之间的相互作用引起的,或者它们纯粹是形态学上的差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/99cb89becb8f/fphys-08-00732-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/937b0e8b0a7b/fphys-08-00732-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/3b1414a9272a/fphys-08-00732-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/be5225c6b070/fphys-08-00732-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/dd312520bf52/fphys-08-00732-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/41f4ad1b0771/fphys-08-00732-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/99cb89becb8f/fphys-08-00732-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/937b0e8b0a7b/fphys-08-00732-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/3b1414a9272a/fphys-08-00732-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/be5225c6b070/fphys-08-00732-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/dd312520bf52/fphys-08-00732-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/41f4ad1b0771/fphys-08-00732-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dfd/5645524/99cb89becb8f/fphys-08-00732-g0006.jpg

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