Docosahexaenoic acid selectively attenuates induction of vascular cell adhesion molecule-1 and subsequent monocytic cell adhesion to human endothelial cells stimulated by tumor necrosis factor-alpha
| Autor: | Christian Weber, Peter C. Weber, Wolfgang Erl, Angelika Pietsch, Ulrich Danesch |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Docosahexaenoic Acids
Molecular Sequence Data Vascular Cell Adhesion Molecule-1 Biology Monocytes chemistry.chemical_compound medicine Cell Adhesion Humans RNA Messenger Cell adhesion Phospholipids Phospholipase C Base Sequence Cell adhesion molecule Tumor Necrosis Factor-alpha Monocyte NF-kappa B Cell biology Endothelial stem cell Enzyme Activation medicine.anatomical_structure chemistry Biochemistry Docosahexaenoic acid Molecular Probes Type C Phospholipases Fatty Acids Unsaturated Phosphatidylcholines lipids (amino acids peptides and proteins) Arachidonic acid Human umbilical vein endothelial cell Endothelium Vascular Cardiology and Cardiovascular Medicine Cell Adhesion Molecules |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1079-5642 |
| Popis: | Abstract Incorporation of the n-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) but not eicosapentaenoic acid or n-6 arachidonic acid into human umbilical vein endothelial cell (HUVEC) phospholipids dose-dependently reduced tumor necrosis factor–α (TNF-α)–induced surface expression of vascular cell adhesion molecule–1 (VCAM-1). In parallel, DHA inhibited TNF-α–stimulated monocytic U937 cell adhesion to HUVECs but did not affect TNF-α– or interferon gamma–induced expression of intercellular adhesion molecule–1 and endothelial leukocyte adhesion molecule–1 or VCAM-1 induction by interleukin-1β. DHA appeared to attenuate VCAM-1 transcription, as it reduced induction of VCAM-1 mRNA by TNF-α. VCAM-1 induction is regulated by activation of nuclear factor– k B, which can be mediated by a TNF-α–responsive phosphatidylcholine-specific phospholipase C (PC-PLC). Gel-shift analysis showed inhibition of TNF-α–induced nuclear factor– k B mobilization by DHA. While the PC-PLC inhibitor D609 dose-dependently prevented VCAM-1 induction by TNF-α, 1,2-diacyl-glycerol (DAG) stimulated VCAM-1 expression, suggesting that VCAM-1 induction by TNF-α may be mediated by activation of PC-PLC. Treatment with DHA resulted in a fourfold enrichment in PC. In addition, DHA or D609 but not eicosapentaenoic acid or arachidonic acid suppressed activation of PC-PLC by TNF-α, estimated as [ 14 C]DAG synthesis in prelabeled HUVECs. Incorporation of DHA into phospholipids selectively attenuates VCAM-1 induction by TNF-α and subsequent monocytic cell adhesion by inhibition of TNF-α–stimulated PC-PLC activation in HUVECs. |
| Databáze: | OpenAIRE |
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