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首页> 外文期刊>Journal of Biomechanics >Impact of oxidative stress on cellular biomechanics and rho signaling in C2C12 myoblasts
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Impact of oxidative stress on cellular biomechanics and rho signaling in C2C12 myoblasts

机译:C2C12肌细胞中氧化胁迫对细胞生物力学和RHO信号的影响

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Although cells often can tolerate oxidative environments, abnormal oxidative stress has been identified in inflammation, cardiovascular and neurodegenerative diseases, and aging. The impact of oxidative stress on the cellular biomechanics is poorly understood, however. In this study, we used C2C12 myoblasts to investigate the effect of oxidative stress, mimicked by hydrogen peroxide (H2O2), on the cell elasticity (i.e., Young's modulus), viability, and production of intracellular reactive oxygen species (ROS). To better understand the mechanisms underlying the impact of H2O2, we examined various effectors of the Rho signaling pathway, which has been shown to play a key role in the control of cell mechanics. H2O2 decreased the cell stiffness in a dose-dependent manner, caused cell death, and reduced the RhoA expression that was accompanied by down-regulation of a-actin, cytoskeleton-membrane linker proteins (ezrin-radixin-moesion proteins), and focal adhesion. Modulating the Rho signaling by using a Rho activator partially restored the cell stiffness, enhanced the cell viability, and decreased the intracellular ROS level, suggesting a potential intervention strategy to maintain the cellular biomechanical homeostasis and rescue cell damage in the threat of oxidative stresses. (C) 2014 Elsevier Ltd. All rights reserved.
机译:虽然细胞通常可以耐氧化环境,但是在炎症,心血管和神经变性疾病中鉴定了异常的氧化胁迫和老化。然而,氧化应激对细胞生物力学的影响很差。在这项研究中,我们使用C2C12肌细胞探讨氧化应激的影响,通过过氧化氢(H2O2)模拟,对细胞弹性(即杨氏模量),活力和细胞内反应性氧(ROS)的产生。为了更好地理解H2O2的影响的基础,我们检查了RHO信号通路的各种效应器,这已被证明在控制细胞力学控制中发挥关键作用。 H 2 O 2以剂量依赖性方式降低细胞刚度,引起细胞死亡,并降低了伴随着α-肌动蛋白,细胞骨架 - 膜接头蛋白(Ezrin-radixin-Moesion蛋白)和局灶性粘附的下调的rhOA表达。通过使用rhO活化剂的调节Rho信号传导部分恢复细胞刚度,增强了细胞活力,并降低了细胞内ROS水平,表明潜在的干预策略,以维持细胞生物力学稳态和泌尿膜损伤在氧化胁迫威胁中的损伤。 (c)2014年elestvier有限公司保留所有权利。

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