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2‐Chlorohexadecanal and 2‐Chlorohexadecanoic Acid Induce COX‐2 Expression in Human Coronary Artery Endothelial Cells
Author(s) -
Messner Maria C.,
Albert Carolyn J.,
Ford David A.
Publication year - 2008
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-008-3189-y
Subject(s) - metabolite , downregulation and upregulation , endothelial stem cell , chemistry , clinical chemistry , endothelium , medicine , endocrinology , biochemistry , in vitro , gene
2‐Chlorohexadecanal (2‐ClHDA), a 16‐carbon chain chlorinated fatty aldehyde that is produced by reactive chlorinating species attack of plasmalogens, is elevated in atherosclerotic plaques, infarcted myocardium, and activated leukocytes. We tested the hypothesis that 2‐ClHDA and its metabolites, 2‐chlorohexadecanoic acid (2‐ClHA) and 2‐chlorohexadecanol (2‐ClHOH), induce COX‐2 expression in human coronary artery endothelial cells (HCAEC). COX‐2 protein expression increased in response to 2‐ClHDA treatments at 8 and 20 h. 2‐ClHA also increased COX‐2 expression following an 8 h treatment. Quantitative PCR showed that 2‐ClHDA treatment increased COX‐2 mRNA over 8 h, while 2‐ClHA treatment led to a modest increase by 1 h and those levels remained constant over 8 h. 2‐ClHDA led to a significant increase in 6‐keto‐PGF 1α release (a measure of PGI 2 release) by HCAEC. These data suggest that 2‐ClHDA and its metabolite 2‐ClHA, which are produced during leukocyte activation, may alter vascular endothelial cell function by upregulation of COX‐2 expression.