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首页> 外文期刊>Journal of cellular physiology. >Podosome formation impairs endothelial barrier function by sequestering zonula occludens proteins
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Podosome formation impairs endothelial barrier function by sequestering zonula occludens proteins

机译：Podosome形成会损害内皮屏障函数通过回收zonula occludens蛋白质

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Podosomes and tight junctions (TJs) are subcellular compartments that both exist in endothelial cells and localize at cell surfaces. In contrast to the well-characterized role of TJs in maintaining cerebrovascular integrity, the specific function of endothelial podosomes remains unknown. Intriguingly, we discovered cross-talk between podosomes and TJs in human brain endothelial cells. Tight junction scaffold proteins ZO-1 and ZO-2 localize at podosomes in response to phorbol-12-myristate-13-acetate treatment. We found that both ZO proteins are essential for podosome formation and function. Rather than being derived from new protein synthesis, podosomal ZO-1 and ZO-2 are relocated from a pre-existing pool found at the peripheral plasma membrane with enhanced physical interaction with cortactin, a known protein marker for podosomes. Sequestration of ZO proteins in podosomes weakens tight junction complex formation, leading to increased endothelial cell permeability. This effect can be further attenuated by podosome inhibitor PP2. Altogether, our data revealed a novel cellular function of podosomes, specifically, their ability to negatively regulate tight junction and endothelial barrier integrity, which have been linked to a variety of cerebrovascular diseases.
机译：Podosomes和紧密连接(套)在亚细胞的隔间都存在在细胞表面内皮细胞和本地化。与套的良好作用在维护脑血管完整性,内皮podosomes的特定函数仍然是未知的。相声podosomes和套在人类之间大脑内皮细胞。蛋白质ZO-1和在podosomes ZO-2本地化应对phorbol-12-myristate-13-acetate治疗。对于podosome形成和功能。而不是来自新的蛋白质合成、podosomal ZO-1和ZO-2搬迁从一个预先存在的池中发现的外围质膜与增强的物理与cortactin互动,一个已知的蛋白质podosomes标记。蛋白质podosomes削弱了紧密连接复杂的形成,导致增加内皮细胞的通透性。通过podosome抑制剂PP2进一步减弱。总之,我们的数据显示新的细胞podosomes功能,具体地说,他们的负调节紧密连接和能力内皮屏障的完整性,与各种脑血管疾病有关。

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