Apolipoprotein E (apoE) isoforms differentially induce nitric oxide production in endothelial cells.
181 - 187.
Although apolipoprotein E3 (apoE3) is atheroprotective, two common isoforms, apoE2 and apoE4, produce recessive and dominant hyperlipidaemias, respectively. Using a fluorescent assay, we report herein that apoE3 particles secreted from recombinant cells stimulate more nitric oxide release in cultured human EA.hy926 endothelial cells than apoE2 or apoE4 (141% more than controls vs. 61 or 11%). Phosphatidylinositol (PI) 3-kinase inhibitors suppressed the apoE effect, while apoE receptor 2 (apoER2) was tyrosine phosphorylated. We conclude that apoE stimulates endothelial nitric oxide release in an isoform-dependent manner, and propose that tyrosine phosphorylation of apoER2 initiates PI3-kinase signalling and activation of nitric oxide synthase. (C) 2003 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.
|Title:||Apolipoprotein E (apoE) isoforms differentially induce nitric oxide production in endothelial cells|
|Keywords:||apolipoprotein E receptor 2, EA.hy926 cells, nitric oxide synthase, PI3-kinase, tyrosine phosphorylation, HEPARAN-SULFATE PROTEOGLYCANS, CORONARY-HEART-DISEASE, HUMAN-BLOOD-PLATELETS, ALZHEIMERS-DISEASE, E RECEPTOR-2, PLASMA-MEMBRANE, LIPOPROTEIN, EXPRESSION, PARTICLES, SYNTHASE|
|UCL classification:||UCL > School of Life and Medical Sciences
UCL > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > School of Life and Medical Sciences > Faculty of Medical Sciences > Medicine (Division of)
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