期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 164, 期 3, 页码 1049-1061出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)63192-6
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- Wellcome Trust Funding Source: Medline
Preeclampsia is a hypertensive complication of human pregnancy characterized by generalized maternal endothelial cell activation. Circulating pro-inflammatory cytokines derived from the placenta are thought to play a key role. We recently demonstrated that hypoxia-reoxygenation (H/R) of placental tissues in vitro causes equivalent oxidative stress to that seen in preeclampsia. Our aim was to determine whether H/R also increases production of tumor necrosis factor-a (TNF-alpha), and whether conditioned media from samples exposed to H/R causes activation of human umbilical vein endothelial cells (HUVECs). Concentrations of mRNA encoding TNF-alpha were significantly higher in placental tissues subjected to H/R compared to hypoxic or normoxic controls. Although there was no difference in the concentrations of TNF-alpha protein in tissue homogenates, levels of TNF-alpha protein in the medium were significantly higher after WR compared to controls, indicating increased secretion. Furthermore, conditioned medium from samples subjected to WR caused increased expression of E-selectin by HUVECs, and the addition of anti-TNF-alpha antibodies significantly reduced that activation. These results are consistent with our hypothesis that intermittent perfusion of the placenta, secondary to reduced trophoblast invasion, causes increased secretion of TNF-alpha, and that this contributes to the activation of maternal endothelial cells that characterizes preeclampsia.
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