| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print March 6, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00301.2001
Submitted on July 2, 2001
Accepted on February 28, 2002
1 Vascular Bioengineering Laboratory, Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA
2 Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: ralevria{at}bme.jhu.edu.
Production of reactive oxygen species (ROS) by the ischemic tissue after ischemia (I)/reperfusion (RP) is an important factor that contributes to tissue injury. The small GTPase Rac1 mediates the oxidative burst and ROS act on signaling pathways involved in expression of inflammatory genes. Since there is evidence implicating monocytes in the pathogenesis of I/RP injury, our objective was to determine the molecular mechanisms that regulate adhesive interactions between monocytes and hypoxia (H)/reoxygenation (RO)-exposed cultured endothelial cells (ECs). When U937 cells were perfused over human umbilical vein ECs at 1 dyn/cm2, H (1 h at 1% O2)/RO (13 h) significantly increased the fluxes of rolling and stably adherent U937 cells. Either EC treatment with the antioxidant pyrrolidine dithiocarbamate (PDTC) or infection with AdRac1N17, that results in expression of the dominant negative form of Rac1, abolished H/RO-induced ROS production, attenuated rolling and abolished stable adhesion of U937 cells to H/RO-exposed ECs. Infection with AdRac1N17 also abolished H/RO-induced upregulation of vascular cell adhesion molecule (VCAM)-1. In turn, blocking VCAM-1 abolished U937 cell stable adhesion and slightly increased rolling. We concluded that the Rac1-dependent ROS partially regulate rolling and exclusively regulate stable adhesion of monocytic cells to ECs after H/RO, and that stable adhesion, but not rolling, is mediated by ROS-induced expression of VCAM-1.
This article has been cited by other articles:
|
|
 |
|
  C. I. Jones III, Z. Han, T. Presley, S. Varadharaj, J. L. Zweier, G. Ilangovan, and B. R. Alevriadou Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite Am J Physiol Cell Physiol, July 1, 2008; 295(1): C180 - C191. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Cernuda-Morollon and A. J. Ridley Rho GTPases and Leukocyte Adhesion Receptor Expression and Function in Endothelial Cells Circ. Res., March 31, 2006; 98(6): 757 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-Y. Sun, N.-P. Wang, F. Kerendi, M. Halkos, H. Kin, R. A. Guyton, J. Vinten-Johansen, and Z.-Q. Zhao Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1900 - H1908. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. F. Wang, X. Zhang, and J. E. Groopman Activation of Vascular Endothelial Growth Factor Receptor-3 and Its Downstream Signaling Promote Cell Survival under Oxidative Stress J. Biol. Chem., June 25, 2004; 279(26): 27088 - 27097. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. van Wetering, N. van den Berk, J. D. van Buul, F. P. J. Mul, I. Lommerse, R. Mous, J.-P. t. Klooster, J.-J. Zwaginga, and P. L. Hordijk VCAM-1-mediated Rac signaling controls endothelial cell-cell contacts and leukocyte transmigration Am J Physiol Cell Physiol, August 1, 2003; 285(2): C343 - C352. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
