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肌纤维细胞和心肌细胞之间的机械合减缓了纤维细胞单层中的电导

Susan A Thompson¹, Craig R Copeland, Daniel H Reich

¹Department of Biomedical Engineering, The Johns Hopkins University, 720 Rutland Ave, Baltimore, MD 21205, USA.

|May 4, 2011

概括

心脏肌纤维细胞在受伤后对心肌细胞施加收缩力,通过机电反损害电导. 阻断肌纤维细胞收缩或机械敏感通道可以恢复纤维化心脏组织的正常电传播.

科学领域:

心脏病学心脏病学
电子生理学电子生理学
生物物理学的生物物理.

背景情况:

心脏肌纤维细胞在受伤后被激活,可以影响心脏组织电生理学.
通过粘附结的机械合方便了细胞间的通信.
肌纤维细胞可能会对心肌细胞施加收缩力,通过机电反影响电传播.

研究的目的:

为了测试肌纤维细胞通过机电反影响心脏电传播的假设.
研究肌纤维细胞收缩和机械敏感通道在受伤后心脏电生理学中的作用.

主要方法:

与肌纤维细胞共同培养新生小鼠心室细胞,并用转化生长因子-β进行治疗以诱导纤维化.
电生理学参数的光学映射 (导电速度,动力潜力的上升冲击速度).
抑制肌纤维细胞收缩 (blebbistatin) 和阻断机械敏感通道 (gadolinium,链杆菌素).
连接43静音和引力测量.

主要成果:

与对照组相比,纤维单层显示出明显降低的纵向和横向导电速度和动作潜力的上升速度.
抑制肌纤维细胞收缩或机械敏感通道在纤维单层中大大增加了导电速度和动力潜力的上升速度.
引力测量表明肌纤维细胞收缩性增加,转化生长因子-β,由blebbistatin降低.

结论:

肌纤维细胞-肌细胞机械相互作用在心脏损伤期间增加.
由于由肌纤维细胞诱导的肌细胞张力增强机械敏感通道激活,心脏导电受损.
针对这些机电反通路可能为创伤后心脏功能障碍提供治疗策略.

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