Problem: Endometriosis is an estrogen-dependent inflammatory disease. Progestins are a first-line treatment for endometriosis via activation of pituitary progesterone receptors and suppression of systemic estrogen: a less than optimal treatment. Increasing evidence is beginning to show that progestins may also influence local endometriotic cells, which may contribute to their clinical efficacy. Method of study: Endometrial stromal cells (ESC) isolated from women with endometriosis were cultured with TNF-α to simulate an inflammatory environment. ESC were treated with the progestins, medroxyprogesterone acetate (MPA), norethisterone acetate (NETA), or dienogest (DNG) and cytokine mRNA production, protein secretion, and cell viability measured. Results: DNG, NETA, and MPA suppressed the secretion of interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1 from ESC. DNG and NETA only reduced the TNF-α-stimulated mRNA production. All three progestins suppressed TNF-α-stimulated ESC proliferation. Conclusion: Progestins may influence endometriotic stromal cells altering the inflammatory microenvironment and their clinical efficacy.

Progestin suppressed inflammation and cell viability of tumor necrosis factor-α-stimulated endometriotic stromal cells / Grandi, Giovanni; Mueller, Michael; Bersinger, Nick; Papadia, Andrea; Nirgianakis, Konstatinos; Cagnacci, Angelo; Mckinnon, Brett. - In: AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY. - ISSN 1046-7408. - STAMPA. - 76:4(2016), pp. 292-298. [10.1111/aji.12552]

Progestin suppressed inflammation and cell viability of tumor necrosis factor-α-stimulated endometriotic stromal cells

GRANDI, GIOVANNI;CAGNACCI, Angelo;
2016

Abstract

Problem: Endometriosis is an estrogen-dependent inflammatory disease. Progestins are a first-line treatment for endometriosis via activation of pituitary progesterone receptors and suppression of systemic estrogen: a less than optimal treatment. Increasing evidence is beginning to show that progestins may also influence local endometriotic cells, which may contribute to their clinical efficacy. Method of study: Endometrial stromal cells (ESC) isolated from women with endometriosis were cultured with TNF-α to simulate an inflammatory environment. ESC were treated with the progestins, medroxyprogesterone acetate (MPA), norethisterone acetate (NETA), or dienogest (DNG) and cytokine mRNA production, protein secretion, and cell viability measured. Results: DNG, NETA, and MPA suppressed the secretion of interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1 from ESC. DNG and NETA only reduced the TNF-α-stimulated mRNA production. All three progestins suppressed TNF-α-stimulated ESC proliferation. Conclusion: Progestins may influence endometriotic stromal cells altering the inflammatory microenvironment and their clinical efficacy.
2016
76
4
292
298
Progestin suppressed inflammation and cell viability of tumor necrosis factor-α-stimulated endometriotic stromal cells / Grandi, Giovanni; Mueller, Michael; Bersinger, Nick; Papadia, Andrea; Nirgianakis, Konstatinos; Cagnacci, Angelo; Mckinnon, Brett. - In: AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY. - ISSN 1046-7408. - STAMPA. - 76:4(2016), pp. 292-298. [10.1111/aji.12552]
Grandi, Giovanni; Mueller, Michael; Bersinger, Nick; Papadia, Andrea; Nirgianakis, Konstatinos; Cagnacci, Angelo; Mckinnon, Brett
File in questo prodotto:
File Dimensione Formato  
AmJReprodImmuno2016-2.pdf

Accesso riservato

Tipologia: Versione pubblicata dall'editore
Dimensione 491.4 kB
Formato Adobe PDF
491.4 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1109148
Citazioni
  • ???jsp.display-item.citation.pmc??? 13
  • Scopus 39
  • ???jsp.display-item.citation.isi??? 35
social impact