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Deletion of the orphan nuclear receptor COUP-TFII in uterus leads to placental deficiency.子宫中孤儿核受体COUP-TFII的缺失会导致胎盘发育不全。
Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6293-8. doi: 10.1073/pnas.0702039104. Epub 2007 Apr 2.
2
Essential roles of COUP-TFII in Leydig cell differentiation and male fertility.COUP-TFII在睾丸间质细胞分化和雄性生育中的重要作用。
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COUP-TFII mediates progesterone regulation of uterine implantation by controlling ER activity.COUP-TFII通过控制雌激素受体（ER）活性介导孕酮对子宫着床的调节。
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4
Suppression of ERalpha activity by COUP-TFII is essential for successful implantation and decidualization.COUP-TFII对雌激素受体α（ERα）活性的抑制作用对于成功着床和蜕膜化至关重要。
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5
The INSL3 gene is a direct target for the orphan nuclear receptor, COUP-TFII, in Leydig cells.胰岛素样肽3（INSL3）基因是睾丸间质细胞中孤儿核受体COUP-TFII的直接作用靶点。
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Orphan nuclear receptor chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) protein negatively regulates bone morphogenetic protein 2-induced osteoblast differentiation through suppressing runt-related gene 2 (Runx2) activity.孤儿核受体鸡卵清蛋白上游启动子转录因子 II（COUP-TFII）蛋白通过抑制 runt 相关基因 2（Runx2）活性负调控骨形态发生蛋白 2 诱导的成骨细胞分化。
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COUP-TFII regulates early bipotential gonad signaling and commitment to ovarian progenitors.COUP-TFII调节早期双潜能性腺信号传导以及向卵巢祖细胞的定向分化。
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Heterozygous rare variants in NR2F2 cause a recognizable multiple congenital anomaly syndrome with developmental delays.NR2F2 中的杂合性罕见变异导致具有发育迟缓的可识别多发性先天性异常综合征。
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7
COUP-TFII in Kidneys, from Embryos to Sick Adults.从胚胎到患病成人，肾脏中的COUP-TFII
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Identification of novel genes and pathways regulated by the orphan nuclear receptor COUP-TFII in mouse MA-10 Leydig cells†.鉴定孤儿核受体 COUP-TFII 在小鼠 MA-10 间质细胞中调控的新基因和通路。
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Decidual NR2F2-Expressing CD4 T Cells Promote TH2 Transcriptional Program During Early Pregnancy.蜕膜中表达 NR2F2 的 CD4 T 细胞在妊娠早期促进 TH2 转录程序。
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本文引用的文献

1
Determinants of trophoblast lineage and cell subtype specification in the mouse placenta.小鼠胎盘中滋养层细胞谱系和细胞亚型特异性的决定因素。
Dev Biol. 2005 Aug 1;284(1):12-24. doi: 10.1016/j.ydbio.2005.05.010.
2
Haploinsufficiency of chicken ovalbumin upstream promoter transcription factor II in female reproduction.鸡卵清蛋白上游启动子转录因子II在雌性生殖中的单倍剂量不足。
Mol Endocrinol. 2005 Sep;19(9):2299-308. doi: 10.1210/me.2005-0019. Epub 2005 May 12.
3
How to make a placenta: mechanisms of trophoblast cell differentiation in mice--a review.如何形成胎盘：小鼠滋养层细胞分化机制——综述
Placenta. 2005 Apr;26 Suppl A:S3-9. doi: 10.1016/j.placenta.2005.01.015.
4
COUP-TFII is essential for radial and anteroposterior patterning of the stomach.COUP-TFII对胃的径向和前后模式形成至关重要。
Development. 2005 May;132(9):2179-89. doi: 10.1242/dev.01808.
5
Pathophysiology of histological changes in early pregnancy loss.早期妊娠丢失组织学改变的病理生理学
Placenta. 2005 Feb-Mar;26(2-3):114-23. doi: 10.1016/j.placenta.2004.05.011.
6
The nuclear orphan receptor COUP-TFII is required for limb and skeletal muscle development.核孤儿受体COUP-TFII是肢体和骨骼肌发育所必需的。
Mol Cell Biol. 2004 Dec;24(24):10835-43. doi: 10.1128/MCB.24.24.10835-10843.2004.
7
The nuclear orphan receptor COUP-TFI is important for differentiation of oligodendrocytes.核孤儿受体COUP-TFI对少突胶质细胞的分化很重要。
Dev Biol. 2004 Feb 15;266(2):238-51. doi: 10.1016/j.ydbio.2003.10.038.
8
SOCS3: an essential regulator of LIF receptor signaling in trophoblast giant cell differentiation.细胞因子信号转导抑制因子3：滋养层巨细胞分化过程中白血病抑制因子受体信号传导的关键调节因子。
EMBO J. 2003 Feb 3;22(3):372-84. doi: 10.1093/emboj/cdg057.
9
Requirement of Bmpr1a for Müllerian duct regression during male sexual development.雄性性发育过程中苗勒氏管退化对Bmpr1a的需求。
Nat Genet. 2002 Nov;32(3):408-10. doi: 10.1038/ng1003. Epub 2002 Oct 7.
10
COUP-TFI: an intrinsic factor for early regionalization of the neocortex.COUP-TFI：新皮质早期区域化的内在因素。
Genes Dev. 2001 Aug 15;15(16):2054-9. doi: 10.1101/gad.913601.

子宫中孤儿核受体COUP-TFII的缺失会导致胎盘发育不全。

Deletion of the orphan nuclear receptor COUP-TFII in uterus leads to placental deficiency.

作者信息

Petit Fabrice G, Jamin Soazik P, Kurihara Isao, Behringer Richard R, DeMayo Francesco J, Tsai Ming-Jer, Tsai Sophia Y

机构信息

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6293-8. doi: 10.1073/pnas.0702039104. Epub 2007 Apr 2.

DOI:10.1073/pnas.0702039104
PMID:17404209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1851059/
Abstract

COUP-TFII (NR2F2), chicken ovalbumin upstream promoter-transcription factor II, is an orphan nuclear receptor of the steroid/thyroid hormone receptor superfamily. The Coup-tfII-null mutant mice die during the early embryonic development because of angiogenesis and heart defects. To analyze the physiological function of COUP-TFII during organogenesis, we used the cre/loxP system to conditionally inactivate COUP-TFII in the ovary and uterus. Homozygous adult female mutants with specific inactivation of the Coup-tfII gene in uterine stromal and smooth muscle cells have severely impaired placental formation, leading to miscarriage at days 10-12 of pregnancy. Deletion of the Coup-tfII gene resulted in an increase in trophoblast giant cell differentiation, a reduction of the spongiotrophoblast layer, and an absence of labyrinth formation causing an improper vascularization of the placenta. This study describes an important maternal role of COUP-TFII in regulating the placentation. The endometrial COUP-TFII might modulate the signaling between the uterus and the extraembryonic tissue for the proper formation of the placenta.

摘要

COUP-TFII（NR2F2），即鸡卵清蛋白上游启动子转录因子II，是类固醇/甲状腺激素受体超家族的一种孤儿核受体。Coup-tfII基因敲除突变小鼠在胚胎发育早期因血管生成和心脏缺陷而死亡。为了分析COUP-TFII在器官发生过程中的生理功能，我们使用cre/loxP系统在卵巢和子宫中条件性地使COUP-TFII失活。子宫基质和平滑肌细胞中Coup-tfII基因特异性失活的纯合成年雌性突变体胎盘形成严重受损，导致妊娠第10 - 12天流产。Coup-tfII基因的缺失导致滋养层巨细胞分化增加、海绵滋养层变薄以及迷路形成缺失，从而导致胎盘血管化异常。本研究描述了COUP-TFII在调节胎盘形成过程中的重要母体作用。子宫内膜中的COUP-TFII可能调节子宫与胚外组织之间的信号传导，以促进胎盘的正常形成。