Effect of transient TCDD exposure on immortalized human trophoblast-derived cell lines
Effect of transient TCDD exposure on immortalized human trophoblast-derived cell lines
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DOI：
10.1177/0960327111424305
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发表时间：
2012-06-01
影响因子：
2.8
通讯作者：
Wake, N.
中科院分区：
文献类型：
--
作者：
Fukushima, K.;Tsukimori, K.;Wake, N.
出生前接触低水平二恶英与出生体重低有关，而出生体重低又与长期后遗症有关。我们将人绒毛外细胞滋养层（EVT）细胞系HTR-8/SV 40和TCLI暴露于2，3，7，8-四氯二苯并-p-二恶英（TCDD），并评估细胞生长、侵袭和分化。TCDD在Matrigel中对细胞增殖、侵袭或管形成没有影响。EVT衍生细胞表达功能性芳香烃受体蛋白;然而，TCDD暴露并没有改变参与妊娠早期EVT分化的蛋白质的表达水平，包括缺氧诱导因子IA（HIFIA），血管内皮生长因子（VEGF），整合素AI，A6和AVB 3。这些结果表明，二恶英引起的胎儿体重下降不是通过EVT功能障碍引起的血管重塑的结果。
Low level, antenatal exposure to dioxins is associated with low birth weight, which in turn is associated with long-term sequelae. We exposed the human extravillous cytotrophoblast (EVT) lines HTR-8/SV40 and TCLI to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and assessed cell growth, invasion, and differentiation. TCDD had no effect on cell proliferation, invasion, or tube formation in Matrigel. The EVT-derived cells expressed a functional aryl hydrocarbon receptor protein; however, TCDD exposure did not alter expression levels of proteins involved in EVT differentiation in early pregnancy, including hypoxia-inducible factor IA (HIFIA), vascular endothelial growth factor (VEGF), Integrin AI, A6, and AVB3. These results suggest that the reduction in fetal weight induced by dioxin is not the result of vascular remodeling via EVT dysfunction.