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Impact of lipid rafts on modulation of intramonocyte calcium‐signalling and adhesion of monocytes to endothelial cells by n‐3 and n‐6 fatty acids
Author(s) -
Schaefer Martina Barbara,
Schaefer Christian Alexander,
Völker Stephanie M,
Fehsecke Annett,
Most Astrid Kerstin,
Neumann Thomas,
Bi Ming H,
Seeger Werner,
Mayer Konstantin,
Erdogan Ali
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1292
Adhesion of monocytes to endothelium is important in inflammation. Cytokines as TNFα induce adhesion by modulation of intracellular calcium signalling and further cellular activation. Recruitment of TNF‐receptor to lipid rafts is crucial in cellular activation by TNFα. Lipid rafts modulate signaltransduction. While n‐6 fatty acids (FA) like arachidonic acid (AA) have proinflammatory properties, n‐3 FA like eicosapentaenic acid (EPA) or docosahexaenic acid (DHA) act antiinflammatory. Aim of this study was to examine, whether lipid rafts are relevant for modulation of inflammatory processes by FA. Measurement of monocyte calcium content and adhesion of U937 to HUVEC was performed using the fluorescence dyes Fura‐2AM and BCECF. Compared to stimulation of U‐937 cells with TNFα, preincubation with EPA or DHA resulted in a decrease of monocyte calcium‐content. AA enhanced adhesion of U‐937 cells to HUVEC compared to n‐3 FA. Preincubation of U‐937 cells with the calciumchelator BAPTA or Xestospongin abolished the differential effect of FA on calcium influx and adhesion. Destruction of monocyte lipid rafts using MCD also prevented the FA‐induced modulation. Contrary to AA, n‐3 FA reduce the TNFα‐induced modulation of calcium influx in monoctes and adhesion to HUVEC. This is abolished after destruction of lipid rafts. Therefore, lipid rafts are of high importance for FA –induced modulation of inflammation.