期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 98, 期 5, 页码 791-804出版社
WILEY
DOI: 10.1189/jlb.3A1014-480R
关键词
Ischemia and reperfusion; apolipoprotein H; eicosanoids
资金
- U.S. National Institutes of Health (NIH) [R01 AI061691, R21 AI107005, P20GM103418]
- American Heart Association
- Kansas State University National Science Foundation GK-12 program
- Kansas State University College of Veterinary Medicine
- Kansas State University
Multiple pathologic conditions, including hemorrhage, tumor angiogenesis, and ischemia-reperfusion events, will result in hypoxia and subsequent reperfusion. Previous studies have analyzed the lipid changes within whole tissues and indicated that ischemia-reperfusion altered tissue and cellular phospholipids. Using an in vitro cell culture model of hypoxia and reoxygenation, we examined the endothelial lipid changes. We hypothesized that phospholipid scramblase 1, a protein that regulates bilayer asymmetry, is involved in altering the phospholipids of endothelial cells during hypoxia, a component of ischemia, leading to beta(2)-glycoprotein I and IgM binding and subsequent lipid-mediated, inflammatory responses. We have completed the first comprehensive study of steady-state phospholipid scramblase 1 mRNA levels, protein expression, and activity under conditions of hypoxia and reoxygenation. Phospholipid scramblase 1 regulates phosphatidylserine exposure in response to oxygen stress, leading to beta(2)-glycoprotein I and IgM binding and lipid-mediated, inflammatory responses.
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