Endothelial progenitor cells and preeclampsia.
Endothelial progenitor cells and preeclampsia.
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DOI：
10.2741/2240
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
H. Gammill;Carol Lin;C. Hubel
中科院分区：
文献类型：
--
作者：
H. Gammill;Carol Lin;C. Hubel
母体对妊娠的心血管适应涉及对生长中的孕体的复杂生理反应，包括母体血管内皮细胞的改变，其导致全身血管阻力的显著下降。有大量的证据表明，血管内皮的不良变化是先兆子痫的多系统母体表现的基础。我们的知识是不完整的机制，正常妊娠的适应性内皮细胞的变化，以及为什么这些变化是减弱或失败的妇女谁发展先兆子痫。骨髓来源的内皮祖细胞（EPCs）群体存在于成人体内，通过雌激素和血管内皮生长因子等刺激动员进入循环。然后，这些EPCs可以分化为血管腔内衬的内皮细胞和/或释放以旁分泌方式起作用以支持内皮的生长因子。因此，EPC被认为是细胞库，以取代功能失调或衰老的内皮细胞，因此可能是血管内皮的整体健康的关键。有数据显示，正常妊娠时母体循环中EPCs的数量增加，而先兆子痫妇女中未发生这种变化。虽然在这一点上推测，我们的总体假设是，过量的抗血管生成因子[如可溶性受体，可溶性fms样酪氨酸激酶（sFlt-1）和可溶性内皮糖蛋白]干扰一氧化氮驱动的动员或活性的内皮祖细胞在母体循环，有助于广泛的内皮功能障碍的先兆子痫的临床表现。
The maternal cardiovascular adaptation to pregnancy involves a complex physiologic response to the presence of the growing conceptus, including alterations in maternal vascular endothelial cells that contribute to a profound fall in total systemic vascular resistance. There is a large body of evidence that adverse changes in the vascular endothelium underlie the multisystemic maternal manifestations of preeclampsia. Our knowledge is incomplete regarding the mechanisms of adaptive endothelial changes of normal pregnancy and why these changes are attenuated or fail in women who develop preeclampsia. Populations of bone-marrow derived endothelial progenitor cells (EPCs) exist in the adult that are mobilized into the circulation by stimuli such as estrogen and vascular endothelial growth factor. These EPCs can then differentiate into endothelial cells lining the lumen of blood vessels and/or release growth factors that act in a paracrine fashion to support the endothelium. EPCs are thus thought to function as a cellular reservoir to replace dysfunctional or senescent endothelial cells, and therefore may be critical to the overall health of the vascular endothelium. Data are emerging to suggest that the number of EPCs in the maternal circulation increases with normal pregnancy and that this change fails to occur in women with preeclampsia. While speculative at this point, our overall hypothesis is that an excess of antiangiogenic factors [such as the soluble receptors, soluble fms-like tyrosine kinase (sFlt-1) and soluble endoglin] interfere with nitric oxide-driven mobilization or activity of EPCs in the maternal circulation, contributing to the widespread endothelial dysfunction underlying the clinical manifestations of preeclampsia.