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Titolo:
Estradiol amplifies interleukin-1-induced monocyte chemotactic protein-1 expression by ectopic endometrial cells of women with endometriosis
Autore:
Akoum, A; Jolicoeur, C; Boucher, A;
Indirizzi:
Univ Laval, Ctr Hosp Univ Quebec, Ctr Rech, Lab Endocrinol Reprod, Quebec City, PQ G1L 3L5, Canada Univ Laval Quebec City PQ Canada G1L 3L5 Quebec City, PQ G1L 3L5, Canada
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 2, volume: 85, anno: 2000,
pagine: 896 - 904
SICI:
0021-972X(200002)85:2<896:EAIMCP>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; PERITONEAL-FLUID; INFERTILE WOMEN; PROGESTERONE RECEPTORS; MILD ENDOMETRIOSIS; OVARIAN-STEROIDS; STROMAL CELLS; SECRETION; MACROPHAGES; ESTROGEN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Akoum, A Hop St Francois Assise, Ctr Rech, Lab Endocrinol Reprod, 10 Rue Espinay,Local D0-711, Quebec City, PQ G1L 3L5, Canada Hop St Francois Assise10 Rue Espinay,Local D0-711 Quebec City PQ Canada G1L 3L5
Citazione:
A. Akoum et al., "Estradiol amplifies interleukin-1-induced monocyte chemotactic protein-1 expression by ectopic endometrial cells of women with endometriosis", J CLIN END, 85(2), 2000, pp. 896-904

Abstract

Endometriosis, one of the most frequently occurring gynecological disorders, is estrogen dependent and is often associated with immunological changes. These include increased macrophage activation and infiltration into the endometriotic implants themselves as well as the peritoneal cavity where theimplants often develop. Despite the critical role estrogens play in the development of endometriosis, the biochemical mechanisms of their action remain unclear. in the present study we report that estradiol (E-2) enhances endometriotic cell responsiveness to the proinflammatory cytokine interleukin-1 beta by up-regulating interleukin-1-induced monocyte chemotactic protein-1 (MCP-1) expression at the level of both protein secretion and messenger ribonucleic acid (mRNA) synthesis, whereas progesterone had no significant effects. According to mRNA half-life experiments, E-2 action does not seem to be due to increased MCP-1 mRNA stability but, rather, to a higher level of transcription, as shown by nm-on analysis. interestingly, immunohistochemical analysis of MCP-1 expression in endometriotic tissue showed intense immunostaining in both epithelial glands and stroma regardless of the menstrual cycle phase, which is consistent with the cell culture data and indicates that MCP-1 expression is not subject to cyclic variation The findings ofthe present study for the first time provide evidence that E-2 upregulates, although in an indirect way, the expression of a potent chemotactic and activating factor by ectopic endometrial cells, which may occur locally in the inflammatory site and contribute to peritoneal macrophage recruitment and activation, and reveal a new means of E-2 action in the pathophysiology of endometriosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 23:31:23