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Coxsackievirus B 3 affects endothelial tight junctions: Possible relationship to ZO‐1 and F‐actin, as well as p38 MAPK activity
Author(s) -
Ju Yuanrong,
Wang Tao,
Li Yang,
Xin Wei,
Wang Shuyun,
Li Jianfeng
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2007.04.003
Subject(s) - mapk/erk pathway , microbiology and biotechnology , p38 mitogen activated protein kinases , umbilical vein , actin , human umbilical vein endothelial cell , flow cytometry , coxsackievirus , tight junction , chemistry , biology , kinase , immunology , biochemistry , in vitro , virus , enterovirus
Tight junction (TJ) plays a pivotal role in preventing the invasion of pathogens from the blood to extracellular environment. However, the mechanisms by which Group B coxsackievirus 3 (CVB 3 ) can get through TJ from the apical surface still remain obscure. In the present study, the human umbilical vein endothelial cell (HUVEC) was utilized to investigate the alterations in F‐actin and ZO‐1 status, permeability as well as p38 mitogen‐activated protein kinase (MAPK) activity in response to CVB 3 by means of fluorescence labeling, flow cytometry, and macromolecule permeability assay. We found that CVB 3 was able to induce reorganization of F‐actin and redistribution of ZO‐1, increase the level of F‐actin, and elevate the permeability of FITC‐albumin. Moreover, CVB 3 ‐mediated the above effects involve in P38 MAPK activation. Our preliminary study indicates that CVB 3 ‐induced alteration in permeability may be attributed to disruption of F‐actin and ZO‐1 organizations and that SB203580, a specific P38 MAPK inhibitor, can reverse these effects. The precise mechanisms underlying the CVB 3 ‐mediated effects on HUVECs need to be studied further.