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[胎膜破裂的生物化学]

[Biochemistry of fetal membranes rupture].

作者信息

Méhats C, Schmitz T, Marcellin L, Breuiller-Fouché M

机构信息

Inserm U1016, institut Cochin, département génétique et développement, faculté de médecine Cochin, 24, rue du Faubourg-Saint-Jacques, 75014 Paris, France.

出版信息

Gynecol Obstet Fertil. 2011 Jun;39(6):365-9. doi: 10.1016/j.gyobfe.2011.04.006. Epub 2011 May 24.

Abstract

Fetal membranes, amnion and chorion, line up the amniotic cavity and are essential for its integrity towards normal term of pregnancy. They consist of a pluristratified structure whose composition assures their cohesion and elasticity. They firstly function in retaining the fluctuant amniotic fluid in a half-rigid cavity. Their elastic limit depends on the organization of the extracellular matrix and firstly on the collagen type it contains. The compact layer of the amnion, responsible for the elastic limit, contains mainly type I collagen, organized in lattice; this allows elongation or spreading. Underneath, the spongy layer, principally of collagen III, is organized in a loose mesh, enriched in hydrated proteoglycans, which allows the absorption of the shocks and the sliding of the amnion on the chorion. The cascade of events leading to the membrane rupture displays: (i) membranes distension with elasticity loss, (ii) separation of the chorion from the amnion, (iii) chorion fracture, (iv) amnion distension which produces an hernia, (v) amnion rupture. The rupture mechanism was long thought to be a consequence of uterine contractions. However, the observation before labour of a zone of altered morphology, with biochemical variations (modifications of metalloprotease activity and of proteoglycans, apoptosis...) associated with focal physical weakness in the region overlying the cervix suggests programming of the rupture before parturition. A better understanding of the biochemical mechanisms of membranes rupture will provide new insights into how to anticipate and to intervene in the case of risk of premature rupture.

摘要

胎膜,即羊膜和绒毛膜,衬于羊膜腔内侧,对于维持孕期直至足月时羊膜腔的完整性至关重要。它们由复层结构组成,其成分确保了它们的黏附性和弹性。它们的首要功能是将波动的羊水保留在半刚性的腔内。其弹性极限取决于细胞外基质的组织方式,首先取决于其中所含的胶原蛋白类型。羊膜的致密层负责弹性极限,主要含有呈晶格状排列的I型胶原蛋白,这使得羊膜能够伸长或伸展。其下方的海绵层主要由III型胶原蛋白组成,呈疏松的网状结构,富含水合蛋白聚糖,能够吸收冲击并使羊膜在绒毛膜上滑动。导致胎膜破裂的一系列事件包括:(i)胎膜扩张并失去弹性,(ii)绒毛膜与羊膜分离,(iii)绒毛膜破裂,(iv)羊膜扩张并形成疝,(v)羊膜破裂。长期以来,人们一直认为破裂机制是子宫收缩的结果。然而,在临产前观察到宫颈上方区域形态改变,伴有生化变化(金属蛋白酶活性和蛋白聚糖的改变、细胞凋亡等)以及局部物理性薄弱,这表明分娩前胎膜破裂存在程序化过程。更好地理解胎膜破裂的生化机制将为如何预测和干预早产风险提供新的见解。

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