Eicosapentaenoic acid protects endothelial cell function injured by hypoxia/reoxygenation.
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.
Morita
I
I
Department of Cellular Physiological Chemistry, Graduate School, Tokyo Medical and Dental University, Japan. morita.cell@tmd.ac.jp
Zhang
Y W
YW
Murota
S I
SI
D002450:Cell Communication / Q000187:drug effects; D015687:Cell Hypoxia / Q000187:drug effects*; D002460:Cell Line; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D017629:Gap Junctions / Q000187:drug effects; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000517:prevention & control*; D013997:Time Factors; D014471:Umbilical Veins
D017382:Reactive Oxygen Species; D015118:Eicosapentaenoic Acid