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首页> 外文期刊>American Journal of Physiology >Deletion of MLCK210 induces subtle changes in vascular reactivity but does not affect cardiac function.
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Deletion of MLCK210 induces subtle changes in vascular reactivity but does not affect cardiac function.

机译：MLCK210的删除引起血管反应性的细微变化，但不影响心脏功能。

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摘要

Myosin light chain kinase (MLCK) plays a key role in the regulation of actomyosin contraction in a large variety of cells. Two isoforms have been described: a short isoform, widely expressed in smooth muscle cells; and a long isoform (MLCK210), mainly localized in the endothelium. This study investigated the consequences on different cardiovascular parameters of MLCK210 gene deletion using MLCK210 knockout mice and of pharmacological inhibition of the kinase using a specific MLCK inhibitor. Deletion of MLCK210 did not affect systolic blood pressure and heart rate or echocardiographic measurements. Electrocardiographic analysis showed neither atrio- nor intraventricular conduction or repolarization defects. Ex vivo responses of aortic rings to vasoconstrictor and vasodilator agonists were not modified in MLCK210 null mice. However, deletion of MLCK210 attenuated shear stress-induced dilation and produced changes in the balance of endothelial-relaxing factors of small mesenteric arteries (SMA). In particular, a reduced flow-mediated NO-dependent dilation was observed. However, it was partially compensated by enhanced indomethacin-sensitive dilation. No significant changes were detected in the endothelium-derived hyperpolarizing component of the vasodilator response. The above effects of MLCK210 gene deletion were confirmed in SMA from wild-type mice by the use of the MLCK enzymatic inhibitor MMZ-10-057. In summary, deletion of MLCK210 was not associated with abnormalities of main in vivo cardiovascular parameters in mice. This study demonstrates a role for MLCK210 in the regulation of flow-dependent dilation in SMA.
机译：肌球蛋白轻链激酶（MLCK）在多种细胞中的肌动球蛋白收缩调节中起关键作用。已经描述了两种同工型：在平滑肌细胞中广泛表达的短同工型;和长同种型（MLCK210），主要位于内皮细胞中。这项研究调查了使用MLCK210基因敲除小鼠对MLCK210基因缺失的不同心血管参数的影响以及使用特定MLCK抑制剂对激酶的药理抑制作用的结果。 MLCK210的删除不影响收缩压和心率或超声心动图测量。心电图分析未见房室传导或心室内传导或复极化缺陷。在MLCK210无效小鼠中，主动脉环对血管收缩剂和血管扩张剂激动剂的离体反应没有改变。然而，MLCK210的删除减弱了剪切应力引起的扩张，并导致了小肠系膜动脉（SMA）的内皮舒张因子平衡的变化。特别地，观察到减少的流量介导的NO依赖性扩张。然而，它被吲哚美辛敏感的扩张作用部分补偿。在血管舒张反应的内皮源超极化成分中未检测到明显变化。通过使用MLCK酶抑制剂MMZ-10-057，在野生型小鼠的SMA中证实了MLCK210基因缺失的上述作用。总之，MLCK210的缺失与小鼠体内主要心血管参数的异常无关。这项研究证明了MLCK210在调节SMA中依赖于流量的扩张中的作用。

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