Paracrine regulation of endometrial function: Interaction between progesterone and corticotropin-releasing factor (CRF) and activin A

Pasquale Florio, Marco Rossi, Matthildur Sigurdardottir, Pasquapina Ciarmela, Stefano Luisi, Paola Viganò, Daniela Grasso, Giovina Fiore, Luigi Cobellis, Anna Maria Di Blasio, Felice Petraglia

Research output: Contribution to journalArticlepeer-review

Abstract

Under the influence of ovarian steroid hormones, endometrial cells are able to produce a wide variety of growth factors and peptide hormones that are believed to promote: (1) physiological growth and differentiation during the endometrial cycle; (2) decidualization, an essential preparative event for establishment of pregnancy; and (3) pathological growth and differentiation in endometriosis and cancer. Among the local factors produced by the human endometrium, corticotropin-releasing factor (CRF) and activin A have been evaluated in terms of localization and effects. CRF is a neuropeptide expressed by the epithelial and stromal cells of the human endometrium in increasing amounts from the endometrial proliferative to the secretory phase. CRF expression also increases in the pregnant endometrium, from early in the pregnancy until term. CRF-type 1 receptor mRNA is only expressed by stromal cells. Progesterone induces CRF gene expression and release from decidualized cells and CRF decidualizes cultured stromal endometrial cells. Urocortin, a CRF-related peptide, has been identified in endometrial epithelial and stromal cells, and its function is still under investigation. Activin A is a growth factor expressed in increasing amounts throughout endometrial phases by both epithelial and stromal cells. This growth factor is secreted into the uterine cavity with higher levels in the secretory phase. Maternal decidua expresses activin A mRNA in increasing amounts from early pregnancy until term. Human endometrium also expresses activin-A receptors and follistatin, its binding protein. Activin A decidualizes cultured human endometrial stromal cells (an effect reversed by follistatin) and modulates embryonic trophoblast differentiation and adhesion. Activin A is expressed in endometriosis and endometrial adenocarcinoma.

Original languageEnglish
Pages (from-to)801-807
Number of pages7
JournalSteroids
Volume68
Issue number10-13
DOIs
Publication statusPublished - Nov 2003

Keywords

  • Decidualization
  • Endometrial cancer
  • Endometriosis
  • Endometrium
  • Implantation
  • Placenta

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Molecular Biology

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