Regulation of endothelial glutathione by ICAM-1: implications for inflammation C. G. KEVIL * , H. PRUITT † , T. J. KAVANAGH ‡ , J. WILKERSON ‡ , F. FARIN ‡ , D. MOELLERING † , V. M. DARLEY-USMAR ‡ ,|| , D. C. BULLARD § and R. P. PATEL † ,|| ,1 * Department of Pathology, Louisiana State University, Shreveport, Shreveport, Louisiana; † Department of Pathology, University of Alabama at Birmingham, ‡ Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington, USA; and § Department of Genetics and || Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA 1 Correspondence: Department of Pathology University of Alabama at Birmingham, 901 19 th Street South, BMR-2, Room 307, Birmingham, AL 35294, USA. E-mail: patel@path.uab.edu <h3>SPECIFIC AIMS</h3> Inflammation plays a central role in development of vascular dysfunction associated with atherosclerosis. At the molecular level important determinants of endothelial function during the inflammatory process are redox status of the cell and expression of adhesion molecule-1 (ICAM-1). Glutathione (GSH) is an important intracellular antioxidant that determines sensitivity of redox signaling pathways in the cell. Depletion of GSH increases susceptibility of cells to inflammation-induced apoptosis mediated by
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Regulation of endothelial glutathione by ICAM-1: implications for inflammation
KEVIL, C. G.; PRUITT, H.; KAVANAGH, T. J.; WILKERSON, J.; FARIN, F.; MOELLERING, D.; DARLEY-USMAR, V. M.; BULLARD, D. C.; PATEL, R. P.
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, Volume 18 (11): 1321
Fed of American Socs for Experimental Biology – Aug 1, 2004
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