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首页> 外文期刊>Biochemical and Biophysical Research Communications >S100A8 protein attenuates airway hyperresponsiveness by suppressing the contraction of airway smooth muscle
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S100A8 protein attenuates airway hyperresponsiveness by suppressing the contraction of airway smooth muscle

机译:S100A8蛋白通过抑制气道平滑肌的收缩而衰减气道高反应性

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摘要

Airway hyperresponsiveness (AHR) is a major clinical problem in allergic asthma mainly caused by the hypercontractility of airway smooth muscles (ASM). S100A8 is an important member of the 5100 calcium-binding protein family with a potential to regulate cell contractility. Here, we analyze the potential of S100A8 to regulate allergen-induced AHR and ASM contraction. Treatment with recombinant S100A8 (rS100A8) diminished airway hyperresponsiveness in OVA-sensitized rats. ASM contraction assays showed that rS100A8 reduced hypercontractility in both isolated tracheal rings and primary ASM cells treated by acetylcholine. rS100A8 markedly rescued the phosphorylation level of myosin light chain induced by acetylcholine in ASM cells. These results show that rS100A8 plays a protective role in regulating AHR in asthma by inhibiting ASM contraction. These results support S100A8 as a novel therapeutic target to control ASM contraction in asthma.(C) 2017 The Authors. Published by Elsevier Inc.
机译:Airway HyperResponsiveness(AHR)是过敏性哮喘的主要临床问题,主要是由气道平滑肌(ASM)的超差异引起的。 S100A8是5100钙结合蛋白家族的重要成员,其潜力调节细胞收缩性。 在这里,我们分析S100A8的潜力来调节过敏原诱导的AHR和ASM收缩。 用重组S100A8(RS100A8)治疗(RS100A8)在OVA致敏大鼠中减少了气道高反应性。 ASM收缩测定显示RS100A8在乙酰胆碱处理的分离的气管环和伯氏细胞中减少了近分裂性。 RS100A8显着拯救了ASM细胞中乙酰胆碱诱导的肌蛋白轻链的磷酸化水平。 这些结果表明,RS100A8通过抑制ASM收缩来调节哮喘中的AHR的保护作用。 这些结果支持S100A8作为一种新的治疗靶标,以控制哮喘中的ASM收缩。(c)2017作者。 elsevier公司发布

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