Detrimental arterial inflammatory effect of microparticles circulating in preeclamptic women: ex vivo evaluation in human arteries. (24th August 2015)

• Record Type: Journal Article
• Authors: Boisramé‐Helms, Julie; Meziani, Ferhat; Sananès, Nicolas; Boisramé, Thomas; Langer, Bruno; Schneider, Francis; Ragot, Thierry; Andriantsitohaina, Ramaroson; Tesse, Angela
• Is Part Of: Fundamental & clinical pharmacology. Volume 29:Number 5(2015)
• Page Start: 450
• Page End: 461
• Publication Date: 2015-08-24
• Subjects: hypertension -- nitric oxide -- preeclampsia -- pregnancy -- vascular inflammation; Pharmacology -- Periodicals; 615.1
• DOI: 10.1111/fcp.12136
• Languages: English
• ISSNs: 0767-3981

Abstract

Abstract: Elevated plasmatic levels of lympho‐monocyte and platelet microparticles (MPs) have been reported in preeclampsia. Previous studies suggest that MPs could participate in preeclampsia vascular impairment. In this study, we investigated the ex vivo vascular effects of MPs from preeclamptic women on arteries from normotensive pregnant women. Omental arteries were collected from normal pregnant women undergoing cesarean section and incubated during 24 h with MPs from normal pregnant or preeclamptic women. Vascular contraction to serotonin and phenylephrine was studied on a wire myograph with or without pharmacological selective inhibitors of inducible nitric oxide synthase (iNOS) and/or cyclo‐oxygenase‐2 (COX‐2). Expression of iNOS, COX‐2, and NF‐κB and production of superoxide anion and 8‐isoprostane were also assessed by immunohistological or biochemical staining and/or Western blot or ELISA assay, respectively. Microparticles from preeclamptic women, but not those from normal pregnant women, induced hyporeactivity to vasocontracturant agonists in omental arteries. Selective inhibitor of iNOS partially restored this arterial contraction, suggesting that nitric oxide (NO) is involved in vascular contractility alteration. Conversely, COX‐2 induced 8‐isoprostane release, a vasoconstricting metabolite modulating the agonist‐induced contraction. COX‐2 selective inhibitor almost abolished the arterial contraction in the same vessels. Interestingly, the association of iNOS and COX‐2 selective inhibitors restored the contraction to control levels. Moreover, iNOS, COX‐2, and NF‐κB expressions are upregulated and superoxide anion levels increased in vessels incubated with MPs from preeclamptic women. In conclusion, circulating MPs from preeclamptic women induce vascular inflammation and enhance oxidative stress. These results suggest a possible role of MPs during preeclampsia‐induced arterial dysfunction.