CAR modulates E-cadherin dynamics in the presence of adenovirus type 5.
CAR modulates E-cadherin dynamics in the presence of adenovirus type 5.
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DOI：
10.1371/journal.pone.0023056
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Santis G
中科院分区：
文献类型：
--
作者：
Hussain F;Morton PE;Snippe M;Sullivan J;Farmer C;Martin-Fernandez ML;Parsons M;Santis G
腺病毒（Ad）血清型5 （Ad5）纤维与柯萨奇病毒和Ad受体（CAR）竞争性结合，将Ad5附着在靶细胞上，并在Ad5感染的后期破坏细胞连接，促进病毒逃逸。本研究表明，在细胞中添加Ad5后，MCF7和CAR过表达MCF7 （FLCARMCF7）细胞的细胞旁通透性在几分钟内增加。这至少部分是通过改变e -钙粘蛋白的分子动力学来实现的，e -钙粘蛋白是细胞-细胞粘附复合物的关键成分。我们还证明，CAR在FLCARMCF7细胞连接处的存在改变了e -钙粘蛋白迁移率的增加。在细胞中加入Ad5后，早期观察到细胞旁通透性增加，我们假设这可能代表了Ad5可以破坏细胞连接以促进进一步进入其细胞受体的机制。
Adenovirus (Ad) serotype 5 (Ad5) fiber competitively binds to the coxsackievirus and Ad receptor (CAR) to attach Ad5 to target cells and also disrupts cell junctions and facilitates virus escape at a late stage in Ad5 infection. Here we demonstrate that paracellular permeability in MCF7 and CAR overexpressing MCF7 (FLCARMCF7) cells is increased within minutes following the addition of Ad5 to cells. This is brought about, at least in part, by altering the molecular dynamics of E-cadherin, a key component of the cell-cell adhesion complex. We also demonstrate that the increase in E-cadherin mobility is constitutively altered by the presence of CAR at FLCARMCF7 cell junctions. As increased paracellular permeability was observed early after the addition of Ad5 to cells, we postulate that this may represent a mechanism by which Ad5 could disrupt cell junctions to facilitate further access to its cell receptors.
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