Thrombin activation of endometrial endothelial cells: A possible role in intrauterine growth restriction
Thrombin activation of endometrial endothelial cells: A possible role in intrauterine growth restriction
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子宫内膜内皮细胞的凝血酶激活：在子宫内生长受限中的可能作用
DOI：
10.1160/th06-07-0387
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发表时间：
2007
影响因子：
6.7
通讯作者：
C. Lockwood
中科院分区：
文献类型：
--
作者：
G. Krikun;S. Huang;F. Schatz;C. Salafia;C. Stocco;C. Lockwood
Summary Preeclampsia (PE), intrauterine growth restriction (IUGR) and abruption with or without fetal loss are associated with reduced uteroplacental blood flow, decidual vasculopathy, endothelial cell dysfunction, thrombosis, inflammation and hemorrhage. Our hypothesis is that reduced uteroplacental blood flow causes focal decidual hypoxia that generates vascular endothelial growth factor (VEGF). The latter acts directly on decidual endothelial cells to induce aberrant expression of tissue factor (TF), the primary initiator of coagulation. This in turn generates thrombin that induces: i) further TF expression; and ii) inflammatory cytokines. BothVEGF and TF induce aberrant angiogenesis-vessel maintenance reflected by endothelial cell fenestrations and induction of a prothrombotic surface causing both the decidual hemorrhage (i.e.abruption) and thrombosis (i.e.uteroplacental vascular insuf- ficiency) observed in these adverse pregnancy outcomes. This novel hypothesis is supported by our finding of TF expression in decidual endothelium of pregnancies complicated by IUGR and/ or fetal loss. Moreover, treatment of cultured endometrial endothelial cells with VEGF or thrombin induces TF protein and mRNA expression. Quantitative RT-PCR analysis indicates that thrombin enhances (>10-fold) the output of diverse inflammatory cytokines in these cultures. The greatest effect (>2-log) was seen on macrophage inflammatory protein 3 α (MIP3 α ). In vitro, thrombin results in endometrial endothelial cell aggregations and changes in the apoptotic pathway. Thus, we postulate that reductions in uteroplacental flow initiate a cascade of molecular effects leading to hypoxia, thrombosis, inflammation, and endothelial cell dysfunction resulting in untoward pregnancy outcomes.
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DOI：
--
发表时间：
1993
期刊：
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影响因子：
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DOI：
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发表时间：
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期刊：
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影响因子：
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DOI：
--
发表时间：
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The American journal of pathology
影响因子：
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DOI：
10.1210/jcem.77.4.8408448
发表时间：
1993
期刊：
The Journal of clinical endocrinology and metabolism
影响因子：
--
作者：
Lockwood,CJ;Nemerson,Y;Krikun,G;Hausknecht,V;Markiewicz,L;Alvarez,M;Guller,S;Schatz,F
通讯作者：
Schatz,F