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Macrophage migration inhibitory factor is involved in ectopic endometrial tissue growth and peritoneal-endometrial tissue interaction in vivo: a plausible link to endometriosis development.

Abstract

Pelvic inflammation is a hallmark of endometriosis pathogenesis and a major cause of the disease's symptoms. Abnormal immune and inflammatory changes may not only contribute to endometriosis-major symptoms, but also contribute to ectopic endometrial tissue growth and endometriosis development. A major pro-inflammatory factors found elevated in peritoneal fluid of women with endometriosis and to be overexpressed in peritoneal fluid macrophages and active, highly vascularized and early stage endometriotic lesions, macrophage migration inhibitory factor (MIF) appeared to induce angiogenic and inflammatory and estrogen producing phenotypes in endometriotic cells in vitro and to be a possible therapeutic target in vivo. Using a mouse model where MIF-knock out (KO) mice received intra-peritoneal injection of endometrial tissue from MIF-KO or syngeneic wild type (WT) mice and vice versa, our current study revealed that MIF genetic depletion resulted in a marked reduction ectopic endometrial tissue growth, a disrupted tissue structure and a significant down regulation of the expression of major inflammatory (cyclooxygenease-2), cell adhesion (αv and β3 integrins), survival (B-cell lymphoma-2) and angiogenic (vascular endothelial cell growth) factors relevant to endometriosis pathogenesis, whereas MIF add-back to MIF-KO mice significantly restored endometriosis-like lesions number and size. Interestingly, cross-experiments revealed that MIF presence in both endometrial and peritoneal host tissues is required for ectopic endometrial tissue growth and pointed to its involvement in endometrial-peritoneal interactions. This study provides compelling evidence for the role of MIF in endometriosis development and its possible interest for a targeted treatment of endometriosis.

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  • Authors+Show Affiliations

    ,

    Endocrinologie de la Reproduction, Centre Hospitalier Universitaire de Québec, Québec, Québec, Canada.

    ,

    Département d'obstétrique et gynécologie, Faculté de médecine de l'Université Laval, Québec, Québec, Canada.

    ,

    Département d'obstétrique et gynécologie, Faculté de médecine de l'Université Laval, Québec, Québec, Canada.

    ,

    Département d'obstétrique et gynécologie, Faculté de médecine de l'Université Laval, Québec, Québec, Canada.

    Endocrinologie de la Reproduction, Centre Hospitalier Universitaire de Québec, Québec, Québec, Canada; Département d'obstétrique et gynécologie, Faculté de médecine de l'Université Laval, Québec, Québec, Canada.

    Source

    PloS one 9:10 2014 pg e110434

    MeSH

    Analysis of Variance
    Animals
    DNA Primers
    Endometriosis
    Endometrium
    Female
    Histological Techniques
    Intramolecular Oxidoreductases
    Macrophage Migration-Inhibitory Factors
    Mice
    Mice, Knockout
    Microscopy, Fluorescence
    Peritoneum
    Real-Time Polymerase Chain Reaction

    Pub Type(s)

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

    Language

    eng

    PubMed ID

    25329068

    Citation

    Rakhila, Halima, et al. "Macrophage Migration Inhibitory Factor Is Involved in Ectopic Endometrial Tissue Growth and Peritoneal-endometrial Tissue Interaction in Vivo: a Plausible Link to Endometriosis Development." PloS One, vol. 9, no. 10, 2014, pp. e110434.
    Rakhila H, Girard K, Leboeuf M, et al. Macrophage migration inhibitory factor is involved in ectopic endometrial tissue growth and peritoneal-endometrial tissue interaction in vivo: a plausible link to endometriosis development. PLoS ONE. 2014;9(10):e110434.
    Rakhila, H., Girard, K., Leboeuf, M., Lemyre, M., & Akoum, A. (2014). Macrophage migration inhibitory factor is involved in ectopic endometrial tissue growth and peritoneal-endometrial tissue interaction in vivo: a plausible link to endometriosis development. PloS One, 9(10), pp. e110434. doi:10.1371/journal.pone.0110434.
    Rakhila H, et al. Macrophage Migration Inhibitory Factor Is Involved in Ectopic Endometrial Tissue Growth and Peritoneal-endometrial Tissue Interaction in Vivo: a Plausible Link to Endometriosis Development. PLoS ONE. 2014;9(10):e110434. PubMed PMID: 25329068.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Macrophage migration inhibitory factor is involved in ectopic endometrial tissue growth and peritoneal-endometrial tissue interaction in vivo: a plausible link to endometriosis development. AU - Rakhila,Halima, AU - Girard,Karine, AU - Leboeuf,Mathieu, AU - Lemyre,Madeleine, AU - Akoum,Ali, Y1 - 2014/10/17/ PY - 2014/03/24/received PY - 2014/06/30/accepted PY - 2014/10/21/entrez PY - 2014/10/21/pubmed PY - 2015/10/16/medline SP - e110434 EP - e110434 JF - PloS one JO - PLoS ONE VL - 9 IS - 10 N2 - Pelvic inflammation is a hallmark of endometriosis pathogenesis and a major cause of the disease's symptoms. Abnormal immune and inflammatory changes may not only contribute to endometriosis-major symptoms, but also contribute to ectopic endometrial tissue growth and endometriosis development. A major pro-inflammatory factors found elevated in peritoneal fluid of women with endometriosis and to be overexpressed in peritoneal fluid macrophages and active, highly vascularized and early stage endometriotic lesions, macrophage migration inhibitory factor (MIF) appeared to induce angiogenic and inflammatory and estrogen producing phenotypes in endometriotic cells in vitro and to be a possible therapeutic target in vivo. Using a mouse model where MIF-knock out (KO) mice received intra-peritoneal injection of endometrial tissue from MIF-KO or syngeneic wild type (WT) mice and vice versa, our current study revealed that MIF genetic depletion resulted in a marked reduction ectopic endometrial tissue growth, a disrupted tissue structure and a significant down regulation of the expression of major inflammatory (cyclooxygenease-2), cell adhesion (αv and β3 integrins), survival (B-cell lymphoma-2) and angiogenic (vascular endothelial cell growth) factors relevant to endometriosis pathogenesis, whereas MIF add-back to MIF-KO mice significantly restored endometriosis-like lesions number and size. Interestingly, cross-experiments revealed that MIF presence in both endometrial and peritoneal host tissues is required for ectopic endometrial tissue growth and pointed to its involvement in endometrial-peritoneal interactions. This study provides compelling evidence for the role of MIF in endometriosis development and its possible interest for a targeted treatment of endometriosis. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/25329068/Macrophage_migration_inhibitory_factor_is_involved_in_ectopic_endometrial_tissue_growth_and_peritoneal_endometrial_tissue_interaction_in_vivo:_a_plausible_link_to_endometriosis_development_ L2 - http://dx.plos.org/10.1371/journal.pone.0110434 DB - PRIME DP - Unbound Medicine ER -