Abstract |
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(1alpha) 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.
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Authors | Maria C Messner, Carolyn J Albert, David A Ford |
Journal | Lipids
(Lipids)
Vol. 43
Issue 7
Pg. 581-8
(Jul 2008)
ISSN: 0024-4201 [Print] United States |
PMID | 18493808
(Publication Type: Journal Article)
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Chemical References |
- 2-chlorohexadecanal
- 2-chlorohexadecanoic acid
- Aldehydes
- I-kappa B Proteins
- Palmitic Acids
- Tumor Necrosis Factor-alpha
- Palmitic Acid
- 6-Ketoprostaglandin F1 alpha
- Cyclooxygenase 2
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Topics |
- 6-Ketoprostaglandin F1 alpha
(metabolism)
- Aldehydes
(pharmacology)
- Blotting, Western
- Cells, Cultured
- Coronary Vessels
(cytology, drug effects)
- Cyclooxygenase 2
(genetics, metabolism)
- Endothelial Cells
(drug effects, enzymology)
- Gene Expression Regulation
(drug effects)
- Humans
- I-kappa B Proteins
(metabolism)
- Palmitic Acid
(pharmacology)
- Palmitic Acids
(pharmacology)
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction
(drug effects)
- Tumor Necrosis Factor-alpha
(pharmacology)
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