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妊娠高血压疾病患者胎盘和血清中非双层磷脂排列及其抗体的测定

Determination of non-bilayer phospholipid arrangements and their antibodies in placentae and sera of patients with hypertensive disorders of pregnancy.

作者信息

Campos B, Chames M, Lantry J M, Bill J P, Eis A, Brockman D, Neil J, Tischner E, Barton J, Wong C, Schwemberger S, Cornelius J, Myatt L, Baeza I, Hnat M

机构信息

Department of Obstetrics and Gynecology, College of Medicine, University of Cincinnati, 231 Albert Sabin, Cincinnati, OH 45267-0526, USA.

出版信息

Placenta. 2006 Feb-Mar;27(2-3):215-24. doi: 10.1016/j.placenta.2005.01.010.

DOI:10.1016/j.placenta.2005.01.010
PMID:16338467
Abstract

Studies suggest that preeclampsia (PE) originates in the placenta and is associated with deficient trophoblast invasion of spiral arteries. The direct cause remains unknown, but preeclampsia is often associated with circulating factors that can induce generalized endothelial dysfunction. Antiphospholipid antibodies (APA) in circulation are also associated with vascular diseases. Although the quantification of APA is not currently used as a prognostic of the risk of PE, studies suggest that thrombophilias play a role in PE pathogenesis. In fact, the pathology of placentae from PE and Antiphospholipid syndrome patients is similar; atherosis, thrombosis and infarction, and endothelium activation represent the pathological mechanisms. We identified a new antibody which recognizes non-bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, and which triggered an autoimmune-like disease in mice. We evaluated the presence of NPA in the placentae and in sera, and whether NPA induced NPA antibodies in patients with hypertensive disorders of pregnancy (HDP). Results showed increased levels of NPA in the syncytiotrophoblast, extravillous cytotrophoblast, syncytial knots and the amnion epithelial cell membranes of the placenta, as well as increases in NPA and NPA antibodies in sera from HDP patients, when compared with controls. This suggests that NPA derived from placenta could be one of multiple factors associated with pregnancy pathologies.

摘要

研究表明,子痫前期(PE)起源于胎盘,与滋养层对螺旋动脉的侵入不足有关。直接病因尚不清楚,但子痫前期通常与可导致全身性内皮功能障碍的循环因子有关。循环中的抗磷脂抗体(APA)也与血管疾病有关。虽然目前APA的定量未被用作子痫前期风险的预后指标,但研究表明血栓形成倾向在子痫前期的发病机制中起作用。事实上,子痫前期患者和抗磷脂综合征患者胎盘的病理表现相似;动脉粥样硬化、血栓形成和梗死以及内皮激活是其病理机制。我们鉴定出一种新抗体,它能识别膜模型和体内细胞膜中的非双层磷脂排列(NPA),并在小鼠中引发类似自身免疫性的疾病。我们评估了胎盘和血清中NPA的存在情况,以及NPA是否会在妊娠高血压疾病(HDP)患者中诱导产生NPA抗体。结果显示,与对照组相比,胎盘合体滋养层、绒毛外细胞滋养层、合体结节和羊膜上皮细胞膜中的NPA水平升高,HDP患者血清中的NPA和NPA抗体也有所增加。这表明源自胎盘的NPA可能是与妊娠病理相关的多种因素之一。

相似文献

1
Determination of non-bilayer phospholipid arrangements and their antibodies in placentae and sera of patients with hypertensive disorders of pregnancy.妊娠高血压疾病患者胎盘和血清中非双层磷脂排列及其抗体的测定
Placenta. 2006 Feb-Mar;27(2-3):215-24. doi: 10.1016/j.placenta.2005.01.010.
2
Anti-phospholipid antibodies increase non-apoptotic trophoblast shedding: a contribution to the pathogenesis of pre-eclampsia in affected women?抗磷脂抗体增加非凋亡性滋养层细胞脱落:对患子痫前期女性发病机制的一种影响?
Placenta. 2009 Sep;30(9):767-73. doi: 10.1016/j.placenta.2009.06.008. Epub 2009 Jul 23.
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Antibodies to non-bilayer phospholipid arrangements induce a murine autoimmune disease resembling human lupus.针对非双层磷脂排列的抗体可诱发一种类似于人类狼疮的小鼠自身免疫性疾病。
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Obstetric complications of antiphospholipid antibodies.抗磷脂抗体的产科并发症。
Curr Opin Obstet Gynecol. 1997 Dec;9(6):387-90.
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Expression patterns of two serine protease HtrA1 forms in human placentas complicated by preeclampsia with and without intrauterine growth restriction.两种丝氨酸蛋白酶HtrA1形式在伴有或不伴有胎儿生长受限的子痫前期患者胎盘组织中的表达模式
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Placental ischaemia is a consequence rather than a cause of pre-eclampsia.胎盘缺血是子痫前期的一个后果而非病因。
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Antiphospholipid antibodies internalised by human syncytiotrophoblast cause aberrant cell death and the release of necrotic trophoblast debris.抗磷脂抗体被人合体滋养层细胞内化后导致异常的细胞死亡,并释放出坏死的滋养层碎片。
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Preeclampsia: current understanding of the molecular basis of vascular dysfunction.子痫前期:对血管功能障碍分子基础的当前认识
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Divergent trophoblast invasion and apoptosis in placental bed spiral arteries from pregnancies complicated by maternal anemia and early-onset preeclampsia/intrauterine growth restriction.孕期合并母体贫血及早发型子痫前期/胎儿生长受限的胎盘床螺旋动脉中滋养层细胞的侵袭和凋亡存在差异。
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Impaired cytotrophoblast cell-cell fusion is associated with reduced Syncytin and increased apoptosis in patients with placental dysfunction.在胎盘功能障碍患者中,细胞滋养层细胞间融合受损与合胞素减少及细胞凋亡增加有关。
Mol Reprod Dev. 2008 Jan;75(1):175-83. doi: 10.1002/mrd.20729.

引用本文的文献

1
Is the atherosclerotic phenotype of preeclamptic placentas due to altered lipoprotein concentrations and placental lipoprotein receptors? Role of a small-for-gestational-age phenotype.子痫前期胎盘的动脉粥样硬化表型是否由于脂蛋白浓度和胎盘脂蛋白受体改变引起?小胎龄表型的作用。
J Lipid Res. 2013 Oct;54(10):2658-64. doi: 10.1194/jlr.M036699. Epub 2013 Jul 29.