Maternal Tgif is required for vascularization of the embryonic placenta
Maternal Tgif is required for vascularization of the embryonic placenta
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DOI：
10.1016/j.ydbio.2008.04.027
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发表时间：
2008-07-15
影响因子：
2.7
通讯作者：
Wotton, David
中科院分区：
文献类型：
--
作者：
Bartholin, Laurent;Melhuish, Tiffany A.;Wotton, David
哺乳动物的胎盘是母体和胚胎之间交换营养和废物的场所。在人类中，胎盘功能不全可导致胎儿宫内发育迟缓、围产儿死亡和自然流产。我们发现，在C57BL/6J小鼠中，转录辅阻遏子TGIF编码基因的零突变会导致胎盘缺陷。主要缺陷是由于胎儿血管减少导致胎盘血管化减少，以及缝隙连接蛋白Gjb2(Cx26)表达减少。这些缺陷导致TGIF杂合子母亲的部分Tif缺失型胚胎严重生长迟缓，以及TGIF缺失型动物的整体生长迟缓。如果母亲也完全缺乏TGIF功能，并且TGIF基因缺失的母亲来自杂合子TGIF胚胎的胎盘有缺陷，那么胎盘缺陷就会严重得多。胚胎移植实验表明，即使野生型胚胎的胎盘在缺乏母体TGIF的情况下也会受到损害。这些结果表明TGIF在胎盘的正常发育中发挥作用，并提示母体因素在调节胚胎来源的胎盘组织的形态发生中发挥作用。(C)2008 Elsevier Inc.保留所有权利。
The mammalian placenta is the site of exchange of nutrients and waste between mother and embryo. In humans, placental insufficiency can result in intrauterine growth retardation, perinatal death and spontaneous abortion. We show that in C57BL/6J mice a null mutation in the gene encoding the transcriptional corepressor, Tgif, causes placental defects. The major defects are decreased vascularization of the placenta, due to a decrease in the fetal blood vessels, and decreased expression of the gap junction protein Gjb2 (Cx26). These defects result in severe growth retardation in a proportion of Tif null embryos in Tgif heterozygous mothers, and an overall growth delay in Tgif null animals. Placental defects are much more severe if the mother also completely lacks Tgif function, and placentas from heterozygous Tgif embryos are defective in a Tgif null mother. Embryo transfer experiments show that even the placenta from a wild type embryo is compromised in the absence of maternal Tgif These results demonstrate that Tgif functions in the normal development of the placenta, and suggest a role for maternal factors in regulating the morphogenesis of embryonically-derived placental tissues. (c) 2008 Elsevier Inc. All rights reserved.