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首页> 外文期刊>Journal of Molecular and Cellular Cardiology >Nonlinear behaviour of conduction and block in cardiac tissue with heterogeneous expression of connexin 43
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Nonlinear behaviour of conduction and block in cardiac tissue with heterogeneous expression of connexin 43

机译：连接蛋白43异源表达在心脏组织中传导和阻滞的非线性行为

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摘要

Altered gap junctional coupling potentiates slow conduction and arrhythmias. To better understand how heterogeneous connexin expression affects conduction at the cellular scale, we investigated conduction in tissue consisting of two cardiomyocyte populations expressing different connexin levels. Conduction was mapped using microelectrode arrays in cultured strands of foetal murine ventricular myocytes with predefined contents of connexin 43 knockout (Cx43KO) cells. Corresponding computer simulations were run in randomly generated two-dimensional tissues mimicking the cellular architecture of the strands. In the cultures, the relationship between conduction velocity (CV) and Cx43KO cell content was nonlinear. CV first decreased significantly when Cx43KO content was increased from 0 to 50%. When the Cx43KO content was >= 60%, CV became comparable to that in 100% Cx43KO strands. Co-culturing Cx43KO and wild-type cells also resulted in significantly more heterogeneous conduction patterns and in frequent conduction blocks. The simulations replicated this behaviour of conduction. For Cx43KO contents of 10-50%, conduction was slowed due to wavefront meandering between Cx43KO cells. For Cx43KO contents >= 60%, clusters of remaining wild-type cells acted as electrical loads that impaired conduction. For Cx43KO contents of 40-60%, conduction exhibited fractal characteristics, was prone to block, and was more sensitive to changes in ion currents compared to homogeneous tissue. In conclusion, conduction velocity and stability behave in a nonlinear manner when cardiomyocytes expressing different connexin amounts are combined. This behaviour results from heterogeneous current-to-load relationships at the cellular level. Such behaviour is likely to be arrhythmogenic in various clinical contexts in which gap junctional coupling is heterogeneous. (c) 2014 Elsevier Ltd. All rights reserved.
机译：间隙间隙连接偶联的改变增强了慢传导和心律不齐。为了更好地了解异质连接蛋白表达如何在细胞水平上影响传导，我们调查了由表达不同连接蛋白水平的两个心肌细胞群体组成的组织中的传导。使用微电极阵列在具有预定含量的连接蛋白43敲除（Cx43KO）细胞的胎鼠心室肌细胞的培养链中绘制传导图。在模拟链的细胞结构的随机生成的二维组织中进行了相应的计算机模拟。在文化中，传导速度（CV）和Cx43KO细胞含量之间的关系是非线性的。当Cx43KO含量从0％增加到50％时，CV首先显着下降。当Cx43KO含量> = 60％时，CV变得与100％Cx43KO链中的CV相当。 Cx43KO和野生型细胞的共同培养也导致明显更多的异质传导模式和频繁的传导阻滞。模拟复制了这种传导行为。对于10％至5​​0％的Cx43KO含量，由于Cx43KO细胞之间的波前蜿蜒而导致传导减慢。当Cx43KO含量> = 60％时，剩余的野生型细胞簇会充当损害传导的电负载。与均质组织相比，当Cx43KO含量为40-60％时，导电表现出分形特征，易于阻塞，并且对离子电流的变化更敏感。总之，当表达不同连接蛋白量的心肌细胞结合时，传导速度和稳定性表现为非线性。此行为是由于蜂窝级别的电流与负载关系不均引起的。在间隙连接偶联是异质的各种临床情况下，这种行为可能导致心律失常。 （c）2014 Elsevier Ltd.保留所有权利。

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