The tight junction protein CAR regulates cardiac conduction and cell-cell communication.
The tight junction protein CAR regulates cardiac conduction and cell-cell communication.
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DOI：
10.1084/jem.20080897
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发表时间：
2008-09-29
影响因子：
15.3
通讯作者：
Gotthardt, Michael
中科院分区：
文献类型：
--
作者：
Lisewski, Ulrike;Shi, Yu;Wrackmeyer, Uta;Fischer, Robert;Chen, Chen;Schirdewan, Alexander;Juettner, Rene;Rathjen, Fritz;Poller, Wolfgang;Radke, Michael H.;Gotthardt, Michael
柯萨奇病毒-腺病毒受体(CAR)以其在病毒摄取中的作用和作为紧密连接的蛋白质而闻名。它主要在发育中的大脑和心脏表达，并在心脏病心脏重塑时重新诱导。到目前为止，CAR在成人心脏中的生理功能在很大程度上是未知的。我们已经产生了心脏特异的诱导性CAR基因敲除(KO)，发现心房和心室之间的电传导受损，随着CAR的进行性丧失而增加。其潜在机制与紧密连接和缝隙连接的串扰有关，连接蛋白的表达和定位改变影响CAR-KO心肌细胞之间的通讯。我们的结果表明，CAR不仅与病毒摄取和心脏重构有关，而且在兴奋从心房到心室的传播中也具有先前未知的功能，这可以解释心律失常与心脏柯萨奇病毒感染的关系。
The Coxsackievirus-adenovirus receptor (CAR) is known for its role in virus uptake and as a protein of the tight junction. It is predominantly expressed in the developing brain and heart and reinduced upon cardiac remodeling in heart disease. So far, the physiological functions of CAR in the adult heart are largely unknown. We have generated a heart-specific inducible CAR knockout (KO) and found impaired electrical conduction between atrium and ventricle that increased with progressive loss of CAR. The underlying mechanism relates to the cross talk of tight and gap junctions with altered expression and localization of connexins that affect communication between CAR KO cardiomyocytes. Our results indicate that CAR is not only relevant for virus uptake and cardiac remodeling but also has a previously unknown function in the propagation of excitation from the atrium to the ventricle that could explain the association of arrhythmia and Coxsackievirus infection of the heart.
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