Bcl-x is not required for maintenance of follicles and corpus luteum in the postnatal mouse ovary

Gregory Riedlinger, Ryugo Okagaki, Kay Uwe Wagner, Edmund B. Rucker, Takami Oka, Keiko Miyoshi, Jodi A. Flaws, Lothar Hennighausen

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

It has been proposed that Bcl-x is a key survival factor in many cell types, and that the bcl-x gene is activated by the transcription factor Stat5 through cytokine signals. In support of this, it has been demonstrated that the survival of mouse primordial germ cells during embryogenesis depends on the presence of Bcl-x. We have now investigated whether, in the mouse, Bcl-x is required for the postnatal maintenance of follicles and luteal cells, and whether Stat5 activates the bcl-x gene. The bcl-x gene was deleted in these cells within the mouse using Cre-loxP recombination. Loss of the bcl-x gene did not affect the numbers of primordial, primary, and antral follicles. Furthermore, expression of the bcl-x gene in the ovary was independent of Stat5 and its activating hormone, prolactin. To determine whether the prolactin receptor (PrlR), Stat5, and Bcl-x were required for establishment and maintenance of the corpus luteum, we induced pseudopregnancies in the respective gene-deletion mice. Whereas luteal cells underwent apoptosis in the absence of the PrlR, no changes were observed in the absence of Stat5 or Bcl-x.

Original languageEnglish (US)
Pages (from-to)438-444
Number of pages7
JournalBiology of reproduction
Volume66
Issue number2
DOIs
StatePublished - Jan 1 2002

Keywords

  • Apoptosis
  • Corpus luteum
  • Follicle
  • Granulosa cells

ASJC Scopus subject areas

  • Reproductive Medicine
  • Cell Biology

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    Riedlinger, G., Okagaki, R., Wagner, K. U., Rucker, E. B., Oka, T., Miyoshi, K., Flaws, J. A., & Hennighausen, L. (2002). Bcl-x is not required for maintenance of follicles and corpus luteum in the postnatal mouse ovary. Biology of reproduction, 66(2), 438-444. https://doi.org/10.1095/biolreprod66.2.438