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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/29399
Title: 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
Authors: Duangporn Plasen
Pravit Akarasereenont
Kitirat Techatraisak
Sirikul Chotewuttakorn
Athiwat Thaworn
Mahidol University
Keywords: Medicine
Issue Date: 1-Dec-2010
Citation: Journal of the Medical Association of Thailand. Vol.93, No.SUPPL 2 (2010)
Abstract: 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.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=79952266170&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/29399
ISSN: 01252208
Appears in Collections:Scopus 2006-2010

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