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Eicosapentaenoic Acid Protects Endothelial Cell Function Injured by Hypoxia/Reoxygenation
Author(s) -
MORITA IKUO,
ZHANG YOUWEI,
MUROTA SEIITSU
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03971.x
Subject(s) - eicosapentaenoic acid , tyrosine kinase , endothelial stem cell , chemistry , hypoxia (environmental) , pharmacology , protein tyrosine phosphatase , endothelium , endothelial dysfunction , tyrosine , biochemistry , endocrinology , biology , signal transduction , fatty acid , oxygen , polyunsaturated fatty acid , organic chemistry , in vitro
A bstract : Eicosapentaenoic acid (EPA) may protect against atherosclerosis by improving lipid metabolism and modulating vascular cell function. Ischemia/reperfusion injury is one risk factor for atherosclerosis. We investigated if EPA could improve hypoxia/reoxygenation (H/R)‐induced endothelial cell dysfunction of gap junctional intercellular communication (GJIC). GJIC in human umbilical vascular endothelial cells (HUVECs) was measured using a photobleaching technique. Results demonstrated that H (24h)/R 2h) induced a GJIC reduction in HUVECs; however, it was inhibited by EPA pretreatment. H/R produced reactive oxygen species, but it was not affected by EPA, and it contributed little to GJIC dysfunction. By contrast, tyrosine kinase activated by H/R was inhibited by EPA pretreatment, and tyrosine kinase inhibitors also abolished H/R‐induced GJIC reduction. The protective effects of EPA on the H/R‐induced GJIC reduction was also observed in cells treated with tyrosine phosphatase inhibitor. These data indicate the EPA improves H/R‐induced endothelial dysfunction through inhibition of tyrosine kinase activation, and it could lead to prevention of progression and/or initiation of atherosclerosis.