Tags

Type your tag names separated by a space and hit enter

Interleukin-1 stimulates macrophage migration inhibitory factor secretion in ectopic endometrial cells of women with endometriosis.
Am J Reprod Immunol 2007; 58(6):505-13AJ

Abstract

PROBLEM

Macrophage migration inhibitory factor (MIF), a potent immuno-modulatory, angiogenic and tissue remodeling factor, is markedly expressed in ectopic endometrial implants and may play key role in the capability of this tissue to grow and develop into the host tissue. The objective of this study was to determine whether macrophage-derived cytokines, such as interleukin (IL)-1, which is overproduced by endometriosis women's peritoneal macrophages and found in elevated concentration in their peritoneal fluid, may play a role in MIF synthesis and secretion by ectopic endometrial cells.

METHODS OF STUDY

Primary cultures of endometriotic cells exposed to IL-1beta and evaluation of MIF protein by immunocytofluorescence and ELISA, and mRNA by quantitative real-time PCR and nuclear transcription assays (run-on).

RESULTS

Interleukin-1beta acts rapidly on endometriotic cells and stimulated MIF secretion and mRNA steady-state levels in a dose and time-dependent manner. IL-1beta treatment had no significant effect on MIF mRNA half-life and stability, but acted predominantly by up-regulating MIF gene transcription as assessed by run-on.

CONCLUSION

These data clearly indicate that IL-1 can be involved in the up-regulation of MIF expression by ectopic endometrial implants. Such an interaction between IL-1 and MIF may have an important impact on endometriotic cell growth and endometriosis pathophysiology.

Authors+Show Affiliations

Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, Faculté de Médecine, Université Laval, QC, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17997749

Citation

Herrmann Lavoie, Catherine, et al. "Interleukin-1 Stimulates Macrophage Migration Inhibitory Factor Secretion in Ectopic Endometrial Cells of Women With Endometriosis." American Journal of Reproductive Immunology (New York, N.Y. : 1989), vol. 58, no. 6, 2007, pp. 505-13.
Herrmann Lavoie C, Fraser D, Therriault MJ, et al. Interleukin-1 stimulates macrophage migration inhibitory factor secretion in ectopic endometrial cells of women with endometriosis. Am J Reprod Immunol. 2007;58(6):505-13.
Herrmann Lavoie, C., Fraser, D., Therriault, M. J., & Akoum, A. (2007). Interleukin-1 stimulates macrophage migration inhibitory factor secretion in ectopic endometrial cells of women with endometriosis. American Journal of Reproductive Immunology (New York, N.Y. : 1989), 58(6), pp. 505-13.
Herrmann Lavoie C, et al. Interleukin-1 Stimulates Macrophage Migration Inhibitory Factor Secretion in Ectopic Endometrial Cells of Women With Endometriosis. Am J Reprod Immunol. 2007;58(6):505-13. PubMed PMID: 17997749.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-1 stimulates macrophage migration inhibitory factor secretion in ectopic endometrial cells of women with endometriosis. AU - Herrmann Lavoie,Catherine, AU - Fraser,Daibhid, AU - Therriault,Marie-Josée, AU - Akoum,Ali, PY - 2007/11/14/pubmed PY - 2008/3/7/medline PY - 2007/11/14/entrez SP - 505 EP - 13 JF - American journal of reproductive immunology (New York, N.Y. : 1989) JO - Am. J. Reprod. Immunol. VL - 58 IS - 6 N2 - PROBLEM: Macrophage migration inhibitory factor (MIF), a potent immuno-modulatory, angiogenic and tissue remodeling factor, is markedly expressed in ectopic endometrial implants and may play key role in the capability of this tissue to grow and develop into the host tissue. The objective of this study was to determine whether macrophage-derived cytokines, such as interleukin (IL)-1, which is overproduced by endometriosis women's peritoneal macrophages and found in elevated concentration in their peritoneal fluid, may play a role in MIF synthesis and secretion by ectopic endometrial cells. METHODS OF STUDY: Primary cultures of endometriotic cells exposed to IL-1beta and evaluation of MIF protein by immunocytofluorescence and ELISA, and mRNA by quantitative real-time PCR and nuclear transcription assays (run-on). RESULTS: Interleukin-1beta acts rapidly on endometriotic cells and stimulated MIF secretion and mRNA steady-state levels in a dose and time-dependent manner. IL-1beta treatment had no significant effect on MIF mRNA half-life and stability, but acted predominantly by up-regulating MIF gene transcription as assessed by run-on. CONCLUSION: These data clearly indicate that IL-1 can be involved in the up-regulation of MIF expression by ectopic endometrial implants. Such an interaction between IL-1 and MIF may have an important impact on endometriotic cell growth and endometriosis pathophysiology. SN - 1046-7408 UR - https://www.unboundmedicine.com/medline/citation/17997749/Interleukin_1_stimulates_macrophage_migration_inhibitory_factor_secretion_in_ectopic_endometrial_cells_of_women_with_endometriosis_ L2 - https://doi.org/10.1111/j.1600-0897.2007.00471.x DB - PRIME DP - Unbound Medicine ER -