AJP - Heart Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (November 20, 2003). doi:10.1152/ajpheart.00841.2003
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
286/3/H1057    most recent
00841.2003v1
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 (13)
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 September 2, 2003
Accepted on November 13, 2003

Involvement of RhoA and Rho Kinase in Neutrophil-Stimulated Endothelial Hyperpermeability

Jerome W. Breslin1* and Sarah Y. Yuan1

1 Departments of Surgery and Medical Physiology, Cardiovascular Research Institute, The Texas A&M University Health Science Center, Scott and White Memorial Hospital, Temple, TX, USA

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

Neutrophil-induced microvascular leakage is an early event in ischemic and inflammatory heart diseases. The specific signaling paradigm by which neutrophils increase microvascular permeability is not yet established. We investigated whether the small GTPase rhoA and its downstream effector rho kinase mediate neutrophil-stimulated endothelial hyperpermeability. We assessed the effect of neutrophils on rho activity in bovine coronary venular endothelial cells (CVEC) with a rho-GTP pull-down assay. Permeability to FITCalbumin was evaluated using CVEC monolayers. We then tested the role of rho kinase in the permeability response to neutrophils using two structurally distinct pharmacological inhibitors: Y27632 and HA-1077. Furthermore, neutrophilstimulated changes in endothelial F-actin organization were examined with fluorescence microscopy. The results show that C5a-activated neutrophils induced an increase in permeability coupled with rhoA activation in CVEC. Inhibition of rho kinase with either Y-27632 or HA-1077 attenuated the hyperpermeability response. Rho kinase inhibition also attenuated increases in permeability stimulated by neutrophil supernatant. In addition, activated neutrophils caused actin stress fiber formation in CVEC, which was diminished by either Y-27632 or HA-1077. These findings suggest that rhoA and rho kinase are involved in the mediation of neutrophil-induced endothelial actin reorganization and barrier dysfunction.




This article has been cited by other articles:


Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
M. Guo, D. Daines, J. Tang, Q. Shen, R. M. Perrin, Y. Takada, S. Y. Yuan, and M. H. Wu
Fibrinogen-{gamma} C-Terminal Fragments Induce Endothelial Barrier Dysfunction and Microvascular Leak via Integrin-Mediated and RhoA-Dependent Mechanism
Arterioscler Thromb Vasc Biol, March 1, 2009; 29(3): 394 - 400.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. W. Breslin, H. Sun, W. Xu, C. Rodarte, A. B. Moy, M. H. Wu, and S. Y. Yuan
Involvement of ROCK-mediated endothelial tension development in neutrophil-stimulated microvascular leakage
Am J Physiol Heart Circ Physiol, February 1, 2006; 290(2): H741 - H750.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. H. Tinsley, J. W. Breslin, N. R. Teasdale, and S. Y. Yuan
PKC-dependent, burn-induced adherens junction reorganization and barrier dysfunction in pulmonary microvascular endothelial cells
Am J Physiol Lung Cell Mol Physiol, August 1, 2005; 289(2): L217 - L223.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.