EXPRESSION OF CORTICOTROPIN-RELEASING HORMONE AND ITS R1 RECEPTOR IN HUMAN ENDOMETRIAL STROMAL CELLS

Citation
Am. Diblasio et al., EXPRESSION OF CORTICOTROPIN-RELEASING HORMONE AND ITS R1 RECEPTOR IN HUMAN ENDOMETRIAL STROMAL CELLS, The Journal of clinical endocrinology and metabolism, 82(5), 1997, pp. 1594-1597
Citations number
20
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
82
Issue
5
Year of publication
1997
Pages
1594 - 1597
Database
ISI
SICI code
0021-972X(1997)82:5<1594:EOCHAI>2.0.ZU;2-5
Abstract
Corticotropin-releasing hormone (CRH) is a hypothalamic neuropeptide t hat has been identified also in several peripheral tissues, including organs of the reproductive system. In man, CRH is synthesized and rele ased by the gonads, the placenta, maternal decidua, and the epithelial endometrium. So far, CRH has been demonstrated in endometrial stromal cells only after decidualization. The aim of this study was to seek e vidence of the production and secretion of CRH by endometrial stromal cells in different phases of the menstrual cycle and to look for gene expression of the recently identified CRH receptor R1. Total RNA was e xtracted from stromal cells monolayers established from endometrial sa mples collected during both proliferative and secretive phases. After reverse transcription, polymerase chain reaction (PCR) amplification w as carried out using primers specific to CRH and to CRH receptor R1, r esulting in the expected bands, respectively 233 bp for CRH and 274 bp for CRH-R1. The identity of the obtained CRH PCR product was confirme d by restriction enzyme analysis and by Southern blotting. Purificatio n by high performance liquid chromatography (HPLC) of stromal cell cul ture medium revealed a major peak of CRH immunoreactivity coeluting wi th the standard CRH(1-41), thus indicating the secretion of the mature peptide. Our study demonstrates the synthesis and secretion of CRH by endometrial stromal cells at all phases of the menstrual cycle, me al so demonstrate the expression of the CRH receptor R1 gene. It can be h ypothesized that CRH contributes via autocrine/paracrine mechanisms to endometrial physiology.