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首页> 外文期刊>American Journal of Physiology >Myosin light chain phosphorylation and pulmonary endothelial cell hyperpermeability in burns.
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Myosin light chain phosphorylation and pulmonary endothelial cell hyperpermeability in burns.

机译：烧伤中的肌球蛋白轻链磷酸化和肺内皮细胞通透性过高。

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摘要

Major cutaneous burns result in not only localized tissue damage but broad systemic inflammation causing organ system damage distal to the burn site. It is well recognized that many problems result from the release of inflammatory mediators that target vascular endothelial cells, causing organ dysfunction. The pulmonary microvessels are particularly susceptible to functional abnormalities as a direct consequence of exposure to burn-induced inflammatory mediators. Traditional therapeutic intervention is quite often ineffective in treating burn patients suffering from systemic problems. A possible explanation for this ineffectiveness may be that because so many mediators are released, supposedly activating numerous signaling cascades that interact with each other, targeting of upstream factors in these cascades on an individual basis becomes futile. Therefore, if an end-point effector responsible for endothelial dysfunction following burn injury could be identified, it may present a target for intervention. In this study, we identified phosphorylation of myosin light chain (MLC) as a required element of burn plasma-induced hyperpermeability across rat lung microvascular endothelial cell monolayers. In addition, pharmacological inhibition of myosin light chain kinase (MLCK) and Rho kinase as well as transfection of MLCK-inhibiting peptide blocked actin stress fiber formation and MLC phosphorylation in response to burn plasma. The results suggest that blocking MLC phosphorylation may provide therapeutic intervention in burn patients with the goal of alleviating systemic inflammation-induced endothelial dysfunction.
机译：严重的皮肤烧伤不仅会导致局部组织损伤，还会导致广泛的全身性炎症，从而导致烧伤部位远端的器官系统受损。众所周知，许多问题是由靶向血管内皮细胞的炎症介质的释放引起的，从而引起器官功能障碍。肺微血管特别容易受到功能异常的影响，这是暴露于烧伤诱导的炎症介质的直接结果。传统的治疗干预在治疗患有系统性疾病的烧伤患者中常常是无效的。这种无效性的可能解释可能是，由于释放了如此多的介体，据称激活了彼此相互作用的许多信号级联，因此以这些为基础单独针对这些级联中的上游因子变得徒劳无功。因此，如果可以确定烧伤后引起内皮功能障碍的终点效应物，则可能成为干预的目标。在这项研究中，我们确定了肌球蛋白轻链（MLC）的磷酸化是大鼠血浆微血管内皮细胞单层中烧伤血浆诱导的高通透性的必需元素。此外，对肌球蛋白轻链激酶（MLCK）和Rho激酶的药理抑制作用以及对MLCK抑制肽的转染作用均能响应烧伤血浆，从而阻止肌动蛋白应激纤维的形成和MLC磷酸化。结果表明，阻断MLC磷酸化可为烧伤患者提供治疗干预，以减轻全身性炎症引起的内皮功能障碍。

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