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From the Institut Gilbert-Laustriat,* UMR CNRS 7175–LC1, Faculté de Pharmacie, Illkirch; the Service de Réanimation Médicale and the Département de Gynécologie et d’Obstétrique, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg, Strasbourg; INSERM 771–CNRS UMR 6214, Faculté de Médecine, Angers; and INSERM 770 and Institut d’Hématologie et d’Immunologie,¶ Université Louis Pasteur, Strasbourg, France
We investigated the role of microparticles in vascular dysfunction of the multisystemic disorder of preeclampsia in women’s omental arteries or mouse arteries. Preeclamptic women displayed increased circulating levels of leukocyte- and platelet-derived microparticles compared with healthy pregnant individuals. Microparticles from preeclamptic, but not healthy, pregnant women induced ex vivo vascular hyporeactivity to serotonin in human omental arteries and mouse aortas. Hyporeactivity was reversed by a nitric-oxide (NO) synthase inhibitor and associated with increased NO production. In the presence of a cyclooxygenase (COX)-2 inhibitor, serotonin-mediated contraction was partially reduced in arteries treated with healthy microparticles but was abolished after treatment with preeclamptic microparticles. This was associated with increased 8-isoprostane production. Preeclamptic microparticles induced up-regulation of inducible nitric-oxide synthase and COX-2 expression, evoked nuclear factor-
B activation, and enhanced oxidative and nitrosative stress. Interestingly, the microparticles originating most probably from leukocytes were responsible for the COX-2 vasoconstrictor component of preeclamptic microparticles, whereas those of platelet origin were mainly involved in NO release. Moreover, vascular hyporeactivity was observed in arteries taken from mice treated in vivo with preeclamptic microparticles. This study demonstrates pathophysiological relevance and provides a paradoxical effect of preeclamptic microparticles associated with proinflammatory properties on vessels, leading to enhanced NO and superoxide anion levels and counteraction of increased COX-2 metabolites.
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