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肝紧密连接:从病毒进入到癌症转移。

Hepatic tight junctions: from viral entry to cancer metastasis.

出版信息

World J Gastroenterol. 2010 Jan 21;16(3):289-95. doi: 10.3748/wjg.v16.i3.289.

DOI:10.3748/wjg.v16.i3.289
PMID:20082472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2807947/
Abstract

The tight junction (TJ) is a critical cellular component for maintenance of tissue integrity, cellular interactions and cell-cell communications, and physiologically functions as the "great wall" against external agents and the surrounding hostile environment. During the host-pathogen evolution, viruses somehow found the key to unlock the gate for their entry into cells and to exploit and exhaust the host cells. In the liver, an array of TJ molecules is localized along the bile canaliculi forming the blood-biliary barrier, where they play pivotal roles in paracellular permeability, bile secretion, and cell polarity. In pathology, certain hepatic TJ molecules mediate virus entry causing hepatitis infection; deregulation and functional abnormality of the TJ have also been implicated in triggering liver cancer development and metastasis. All these findings shed new insights on the understanding of hepatic TJs in the development of liver disease and provide new clues for potential intervention.

摘要

紧密连接(TJ)是维持组织完整性、细胞间相互作用和细胞间通讯的关键细胞成分,在生理上起着抵御外部因素和周围恶劣环境的“长城”作用。在宿主-病原体进化过程中,病毒找到了打开细胞进入细胞的大门的关键,并利用和耗尽宿主细胞。在肝脏中,一系列 TJ 分子定位于胆小管形成血-胆屏障,在那里它们在细胞旁通透性、胆汁分泌和细胞极性中发挥关键作用。在病理学中,某些肝 TJ 分子介导病毒进入导致肝炎感染;TJ 的失调和功能异常也与触发肝癌发展和转移有关。所有这些发现都为理解肝 TJ 在肝病发展中的作用提供了新的见解,并为潜在的干预提供了新的线索。

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本文引用的文献

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Hepatoma cell density promotes claudin-1 and scavenger receptor BI expression and hepatitis C virus internalization.肝癌细胞密度促进紧密连接蛋白-1和清道夫受体BI的表达以及丙型肝炎病毒的内化。
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The tight junction-associated protein occludin is required for a postbinding step in hepatitis C virus entry and infection.紧密连接相关蛋白闭合蛋白是丙型肝炎病毒进入和感染过程中结合后步骤所必需的。
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