Both these authors contributed equally to this work.
Coxsackievirus B3 affects endothelial tight junctions: Possible relationship to ZO-1 and F-actin, as well as p38 MAPK activity
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 2007 International Federation for Cell Biology
Cell Biology International
Volume 31, Issue 10, pages 1207–1213, October 2007
How to Cite
Ju, Y., Wang, T., Li, Y., Xin, W., Wang, S. and Li, J. (2007), Coxsackievirus B3 affects endothelial tight junctions: Possible relationship to ZO-1 and F-actin, as well as p38 MAPK activity. Cell Biology International, 31: 1207–1213. doi: 10.1016/j.cellbi.2007.04.003
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received 31 January 2007; revised 12 March 2007; accepted 3 April 2007
- p38 MAPK
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 (CVB3) 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 CVB3 by means of fluorescence labeling, flow cytometry, and macromolecule permeability assay. We found that CVB3 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, CVB3-mediated the above effects involve in P38 MAPK activation. Our preliminary study indicates that CVB3-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 CVB3-mediated effects on HUVECs need to be studied further.