2008
DOI: 10.1016/j.placenta.2007.11.016
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Circulating Microparticles in Normal Pregnancy and Pre-Eclampsia

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Cited by 221 publications
(185 citation statements)
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“…In our investigation, the observation of increased signs of apoptosis and cell damage together with the presence of intracellular oedema (Figure 11) in the syncytial layer is in line with the concept that there is more syncytial debris ( Figure 13) shed into maternal space in preeclampsia [19], as apoptosis and cell damage proceeds the shedding of syncytial fragments into maternal lacunae or intervillous space. An increased release of syncytiotrophblasts microparticles (STBM) formed by plasma membrane blebbing during apoptosis are triggered in excess into the maternal circulation [20].…”
Section: Disscussionsupporting
confidence: 87%
“…In our investigation, the observation of increased signs of apoptosis and cell damage together with the presence of intracellular oedema (Figure 11) in the syncytial layer is in line with the concept that there is more syncytial debris ( Figure 13) shed into maternal space in preeclampsia [19], as apoptosis and cell damage proceeds the shedding of syncytial fragments into maternal lacunae or intervillous space. An increased release of syncytiotrophblasts microparticles (STBM) formed by plasma membrane blebbing during apoptosis are triggered in excess into the maternal circulation [20].…”
Section: Disscussionsupporting
confidence: 87%
“…During pregnancy, serum lipoproteins except HDL-C increase considerably 17 and are two-to threetimes higher in PIH. Worldwide, various studies 5,[18][19][20][21][22][23][24] have reported elevated lipid levels in PIH subjects similar to our observations.…”
Section: Discussionmentioning
confidence: 94%
“…Both trigger endothelial dysfunction and severe preeclampsia (34,35). The placental ischemia, reperfusion and associated oxidative stress amplify apoptosis by rupture of syncytial architecture and promote the release into the maternal circulation of several components (syncytiotrophoblast membrane microparticles and an excess of antiangiogenic factors, such as sFlt-1) that stimulate the synthesis of inflammatory cytokines (36)(37)(38). This excessive inflammatory response causes endothelial dysfunction, increased vascular reactivity and coagulopathy that precede the development of symptomatic disease (39).…”
Section: Pathogenesismentioning
confidence: 99%