Publication: Initial response of endothelial cells to acute stimulation with a lipid component: Increase cyclooxygenase activity by induction of COX-2 through activation of tyrosine kinase
No. of Pages/File Size
Journal of the Medical Association of Thailand. Vol.93, No.SUPPL 2 (2010)
Duangporn Plasen, Pravit Akarasereenont, Kitirat Techatraisak, Sirikul Chotewuttakorn, Athiwat Thaworn (2010). Initial response of endothelial cells to acute stimulation with a lipid component: Increase cyclooxygenase activity by induction of COX-2 through activation of tyrosine kinase. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/29399.
Initial response of endothelial cells to acute stimulation with a lipid component: Increase cyclooxygenase activity by induction of COX-2 through activation of tyrosine kinase
Objective: To study the initial response of endothelial cells acutely stimulated with a lipid component in the aspect of cyclooxygenase (COX) function which needed for prostacyclin synthesis, an endogenous antiatherogenic agent secreted from endothelial cells. Material and Method: 25 hydroxycholesterol (25OHC) was used as a representative lipid component for stimulating human umbilical vein endothelial cell (HUVEC) obtained from umbilical cords of healthy newborns with informed consent of their mothers. HUVEC were treated with 25OHC (0.1, 1 or 10 microgram/mL) at times 6, or 24 h. COX activity was measured from amount of 6-keto-PGF1alfa production in the presence of exogenous arachidonic acids (10 micromolar; 10 min) by enzyme immunoassay. The amount of COX-1 and COX-2 protein were detected by Western blot. Cell viability was assessed by using MTT assay. Results: 25OHC induced COX-2 protein production with increasing the activity of COX enzyme in HUVEC without change in amount of COX-1 protein. The induction of COX-2 or increasing in COX activity depended on concentration of 25OHC and time to exposure which seemed to be inhibited by genistein, a specific tyrosine kinase inhibitor. Conclusion: Acute stimulation of HUVEC with 25OHC, an atherosclerotic lipid component, increases the activity of COX by inducing COX-2 expression in a manner that depended on concentration and time. The induction of COX-2 expression might possibly mediated through activation protein tyrosine kinase. These responses may be an initial defensive mechanism of endothelial cells from lipid component attack.