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Am J Physiol Heart Circ Physiol 290: H741-H750, 2006. First published September 19, 2005; doi:10.1152/ajpheart.00238.2005
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Involvement of ROCK-mediated endothelial tension development in neutrophil-stimulated microvascular leakage

Jerome W. Breslin,1,2 Hengrui Sun,1,2 Wenjuan Xu,2 Charles Rodarte,2 Alan B. Moy,3 Mack H. Wu,1,2 and Sarah Y. Yuan1,2

1Department of Surgery, University of California at Davis School of Medicine, Sacramento, California; 2Department of Surgery, Scott and White Memorial Hospital, The Texas A&M University Health Science Center, Temple, Texas; and 3Departments of Internal Medicine and Biomedical Engineering, University of Iowa Medical Center, Iowa City, Iowa

Submitted 14 March 2005 ; accepted in final form 12 September 2005

Neutrophil-induced coronary microvascular barrier dysfunction is an important pathophysiological event in heart disease. Currently, the precise cellular and molecular mechanisms of neutrophil-induced microvascular leakage are not clear. The aim of this study was to test the hypothesis that rho kinase (ROCK) increases coronary venular permeability in association with elevated endothelial tension. We assessed permeability to albumin (Pa) in isolated porcine coronary venules and in coronary venular endothelial cell (CVEC) monolayers. Endothelial barrier function was also evaluated by measuring transendothelial electrical resistance (TER) of CVEC monolayers. In parallel, we measured isometric tension of CVECs grown on collagen gels. Transference of constitutively active (ca)-ROCK protein into isolated coronary venules or CVEC monolayers caused a significant increase in Pa and decreased TER in CVECs. The ROCK inhibitor Y-27632 blocked the ca-ROCK-induced changes. C5a-activated neutrophils (106/ml) also significantly elevated venular Pa, which was dose-dependently inhibited by Y-27632 and a structurally distinct ROCK inhibitor, H-1152. In CVEC monolayers, activated neutrophils increased permeability with a concomitant elevation in isometric tension, both of which were inhibited by Y-27632 or H-1152. Treatment with ca-ROCK also significantly increased CVEC monolayer permeability and isometric tension, coupled with actin polymerization and elevated phosphorylation of myosin regulatory light chain on Thr18/Ser19. The data suggest that during neutrophil activation, ROCK promotes microvascular leakage in association with actin-myosin-mediated tension development in endothelial cells.

microvascular permeability; neutrophil-endothelium interaction; signal transduction; cytoskeleton


Address for reprint requests and other correspondence: J. W. Breslin, UCDMC Dept. of Surgery, Div. of Research, 2805 50th St., Rm. 2411, Sacramento, CA 95817 (e-mail: jwbreslin{at}ucdavis.edu)




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