Developmental and Endocrine Signalling Centre, Division of Basic Medical Sciences, St. George's, University of London, London, UK.
Placenta. 2010 Jun;31(6):465-74. doi: 10.1016/j.placenta.2010.03.002. Epub 2010 Mar 31.
A number of important changes take place in the maternal uterine vasculature during the first few weeks of pregnancy resulting in increased blood flow to the intervillous space. Vascular endothelial and smooth muscle cells are lost from the spiral arteries and are replaced by fetal trophoblast cells. Failure of the vessels to remodel sufficiently is a common feature of pregnancy pathologies such as early pregnancy loss, intrauterine growth restriction and pre-eclampsia. There is evidence to suggest that some vascular changes occur prior to trophoblast invasion, however, in the absence of trophoblasts remodelling of the spiral arteries is reduced. Until recently our knowledge of these events has been obtained from immunohistochemical studies which, although extremely useful, can give little insight into the mechanisms involved. With the development of more complex in vitro models a picture of events at a cellular and molecular level is beginning to emerge, although some caution is required in extrapolating to the in vivo situation. Trophoblasts synthesise and release a plethora of cytokines and growth factors including members of the tumour necrosis factor family. Studies suggest that these factors may be important in regulating the remodelling process by inducing both endothelial and vascular smooth muscle cell apoptosis. In addition, it is evident from studies in other vascular beds that the structure of the vessel is influenced by factors such as flow, changes in the composition of the extracellular matrix, the phenotype of the vascular cells and the local immune cell environment. It is the aim of this review to present our current knowledge of the mechanisms involved in spiral artery remodelling and explore other possible pathways and cellular interactions that may be involved, informed by studies in the cardiovascular field.
在怀孕的头几周内，母体子宫血管会发生许多重要变化，导致绒毛间隙的血流量增加。螺旋动脉中的血管内皮和平滑肌细胞会丢失，并被胎儿滋养层细胞取代。血管不能充分重塑是妊娠病理的一个常见特征，如早期妊娠丢失、宫内生长受限和子痫前期。有证据表明，一些血管变化发生在滋养层浸润之前，然而，在没有滋养层的情况下，螺旋动脉的重塑会减少。直到最近，我们对这些事件的了解都是通过免疫组织化学研究获得的，尽管这些研究非常有用，但对涉及的机制却知之甚少。随着更复杂的体外模型的发展，开始出现细胞和分子水平上的事件图景，尽管在推断体内情况时需要谨慎。滋养层合成并释放大量细胞因子和生长因子，包括肿瘤坏死因子家族的成员。研究表明，这些因子可能通过诱导内皮细胞和血管平滑肌细胞凋亡，在调节重塑过程中发挥重要作用。此外，从其他血管床的研究中可以明显看出，血管的结构受到许多因素的影响，如血流、细胞外基质成分的变化、血管细胞的表型和局部免疫细胞环境。本综述旨在介绍我们目前对螺旋动脉重塑所涉及的机制的认识，并探讨其他可能涉及的途径和细胞相互作用，这些途径和相互作用是受到心血管领域研究的启发。
