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

Pasquale Florio, Florio P, Rossi M, Marco Rossi, Sigurdardottir M, Matthildur Sigurðardóttir, Matthildur Sigurdardottir, Pasquapina Ciarmela, Stefano Luisi, Paola Viganò, Grasso D, Daniela Grasso, Giovina Fiore, Fiore G, Luigi Cobellis, Cobellis L, Anna Maria Di Blasio, Di Blasio AM, Felice Petraglia
Steroids · 2003 · vol. 68(10-13) , pp. 801–807 · doi:10.1016/s0039-128x(03)00137-5 · PMID:14667971 · W2112866481
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This paper investigated the paracrine regulation of endometrial function, specifically focusing on the interactions between progesterone, corticotropin-releasing factor (CRF), and activin A.

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Abstract

Under the influence of ovarian steroid hormones, endometrial cells aer able to produce a wide variety of growth factors and peptide hormones that area 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.

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Condition tags

endometriosis

MeSH descriptors

Activins Corticotropin-Releasing Hormone Endometrium Inhibin-beta Subunits Progesterone Activins Cell Differentiation Cell Division Corticotropin-Releasing Hormone Endometrial Neoplasms Endometrial Neoplasms Endometriosis Endometrium Endometrium Female Humans Inhibin-beta Subunits Peptides Peptides Pregnancy

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