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

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

Research output: Contribution to journalArticlepeer-review

66 Citations (Scopus)


COUP-TFII (NR2F2), chicken ovalbumin upstream promoter-transcription factor II, is an orphan nuclear receptor of the steroid/thyroid hormone receptor superfamily. The Coup-tfll-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-tfll 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-tfll 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.

Original languageEnglish
Pages (from-to)6293-6298
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number15
Publication statusPublished - 2007 Apr 10
Externally publishedYes


  • Placenta
  • Reproduction
  • Trophoblast giant cell

ASJC Scopus subject areas

  • General


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