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首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Crossbridge Recruitment Capacity of Wild-Type and Hypertrophic Cardiomyopathy-Related Mutant Troponin-T Evaluated by X-ray Diffraction and Mechanical Study of Cardiac Skinned Fibers
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Crossbridge Recruitment Capacity of Wild-Type and Hypertrophic Cardiomyopathy-Related Mutant Troponin-T Evaluated by X-ray Diffraction and Mechanical Study of Cardiac Skinned Fibers

机译：X射线衍射和心脏皮纤维力学研究评估野生型和肥厚型心肌病相关突变肌钙蛋白-T的跨桥募集能力

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X-ray diffraction and tension measurement experiments were conducted on rat left ventricular skinned fibers with or without “troponin-T treatment,” which exchanges the endogenous troponin T/I/C complex with exogenous troponin-T. These experiments were performed to observe the structural changes in troponin-T within a fiber elicited by contractile crossbridge formation and investigate the abnormality of hypertrophic cardiomyopathy-related troponin-T mutants. The intensity of the troponin reflection at 1/38.5 nm was decreased significantly by ATP addition after treatment with wild-type or mutant troponin-T, indicating that crossbridge formation affected the conformation of troponin-T. In experiments on cardiac fibers treated with the hypertrophic cardiomyopathy-related mutants E244D- and K247R-troponin-T, treatment with K247R-troponin-T did not recruit contracting actomyosin to a greater extent than wild-type-troponin-T, although a similar drop in the intensity of the troponin reflection occurred. Therefore, the conformational change in K247R-troponin-T was suggested to be unable to fully recruit actomyosin interaction, which may be the cause of cardiomyopathy.
机译：对大鼠左心室皮肤纤维进行了X射线衍射和张力测量实验，该纤维经过或未经过“肌钙蛋白T处理”，将内源性肌钙蛋白T / I / C复合物与外源性肌钙蛋白T交换。进行这些实验以观察由收缩性跨桥形成引起的纤维内肌钙蛋白-T的结构变化，并研究与肥厚型心肌病相关的肌钙蛋白-T突变体的异常。用野生型或突变型肌钙蛋白-T处理后，添加ATP后，肌钙蛋白在1 / 38.5 nm处的反射强度显着降低，表明跨桥形成影响了肌钙蛋白-T的构象。在用肥厚型心肌病相关突变体E244D-和K247R-肌钙蛋白-T治疗的心脏纤维的实验中，与野生型肌钙蛋白-T相比，用K247R-肌钙蛋白-T进行的治疗并未招募收缩性肌动球蛋白。肌钙蛋白反射强度下降。因此，提示K247R-肌钙蛋白-T的构象改变不能完全募集放线菌素相互作用，这可能是心肌病的原因。

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