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EnglishProblem: 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.
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.
| Titolo: | Progestin suppressed inflammation and cell viability of tumor necrosis factor-α-stimulated endometriotic stromal cells |
| Autori: | |
| Data di pubblicazione: | 2016 |
| Rivista: | |
| Citazione: | 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. - 76(2016), pp. 292-298. |
| 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. |
| Handle: | http://hdl.handle.net/11390/1105737 |
| Appare nelle tipologie: | 1.1 Articolo in rivista |
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