AJP - Heart AJP: Endocrinology and Metabolism
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (September 19, 2005). doi:10.1152/ajpheart.00238.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
290/2/H741    most recent
00238.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (11)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Breslin, J. W
Right arrow Articles by Yuan, S. Y
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Breslin, J. W
Right arrow Articles by Yuan, S. Y
Submitted on March 14, 2005
Accepted on September 12, 2005

Involvement of ROCK-mediated endothelial tension development in neutrophil-stimulated microvascular leakage

Jerome W Breslin1*, Hengrui Sun1, Wenjuan Xu2, Charles Rodarte2, Alan B Moy3, Mack H Wu1, and Sarah Y Yuan1

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

* To whom correspondence should be addressed. E-mail: jwbreslin{at}ucdavis.edu.

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 other experiments, we measured isometric tension of CVEC 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 CVEC. 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 MLC on Ser-18/Thr-19. The data suggest that during neutrophil activation, ROCK promotes microvascular leakage in association with actin-myosin mediated tension development in endothelial cells.




This article has been cited by other articles:


Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
N. Gaudreault, R. M. Perrin, M. Guo, C. P. Clanton, M. H. Wu, and S. Y. Yuan
Counter Regulatory Effects of PKC{beta}II and PKC{delta} on Coronary Endothelial Permeability
Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1527 - 1533.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
G. P. van Nieuw Amerongen, R. J. P. Musters, E. C. Eringa, P. Sipkema, and V. W. M. van Hinsbergh
Thrombin-induced endothelial barrier disruption in intact microvessels: role of RhoA/Rho kinase-myosin phosphatase axis
Am J Physiol Cell Physiol, May 1, 2008; 294(5): C1234 - C1241.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
M. Guo, J. W. Breslin, M. H. Wu, C. J. Gottardi, and S. Y. Yuan
VE-cadherin and {beta}-catenin binding dynamics during histamine-induced endothelial hyperpermeability
Am J Physiol Cell Physiol, April 1, 2008; 294(4): C977 - C984.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. H. Adamson, J. C. Ly, R. K. Sarai, J. F. Lenz, A. Altangerel, D. Drenckhahn, and F. E. Curry
Epac/Rap1 pathway regulates microvascular hyperpermeability induced by PAF in rat mesentery
Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1188 - H1196.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
M. Xu, C. L. Waters, C. Hu, R. B. Wysolmerski, P. A. Vincent, and F. L. Minnear
Sphingosine 1-phosphate rapidly increases endothelial barrier function independently of VE-cadherin but requires cell spreading and Rho kinase
Am J Physiol Cell Physiol, October 1, 2007; 293(4): C1309 - C1318.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
F.V. Hartel, C.W. Rodewald, M. Aslam, D. Gunduz, L. Hafer, J. Neumann, H.M. Piper, and T. Noll
Extracellular ATP induces assembly and activation of the myosin light chain phosphatase complex in endothelial cells
Cardiovasc Res, June 1, 2007; 74(3): 487 - 496.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1977 by the American Physiological Society.