The Estrogen Early Response Gene FOS Is Altered in a Baboon Model of Endometriosis1

Julie M. Hastings, Jackson KS, Kevin S. Jackson, Mavrogianis PA, Patricia A. Mavrogianis, Fazleabas AT, Asgerally T Fazleabas
Biology of reproduction · 2006 · vol. 75(2) , pp. 176–182 · doi:10.1095/biolreprod.106.052852 · PMID:16672717 · W2092340366
article OA: bronze CC0 ⤵ 39 in-corpus citations
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Endometriosis in baboons upregulated the estrogen early response gene FOS and other immune-related genes in eutopic endometrium, indicating an altered immunological environment.

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Abstract

Endometriosis, the presence of a functional endometrium outside of the uterine cavity, is associated with infertility. In our simulated model of pregnancy in baboons with experimental endometriosis, hCG infusion fails to induce expression of the immunoregulatory protein glycodelin. To test the hypothesis that the development of endometriosis is associated with an aberrant endometrial immunological environment, we examined the expression of a series of immunoregulatory genes in endometrium from baboons with and without endometriosis. Six months following intraperitoneal inoculation with menstrual endometrium, eutopic endometrium was surgically collected between Days 9 and 11 postovulation. Control endometrium was similarly collected from disease-free animals. Total RNA was extracted, and biotinylated cDNA probes were hybridized to the SuperArray GEArray Q series Th1/Th2/Th3 cDNA array, representing 96 genes. Gene expression levels were determined using ScanAlyze and GEArray Analyzer software. Seven genes were upregulated, including JUND, FOS, CCL11, NFKB1 and others, in the endometrium from baboons with endometriosis compared with the endometrium from disease-free animals; one gene, IL1R1, was downregulated. Quantitative RT-PCR confirmed upregulation of FOS and CCL11 in endometriotic eutopic endometrium. Immunohistochemical analysis revealed altered levels and distribution of FOS protein in the eutopic endometrium of baboons with induced endometriosis. These data suggest that in an induced model of endometriosis an aberrant eutopic immunological environment results in a decreased apoptotic potential and in rapid alterations in endometrial gene expression. We propose that the reduced fecundity associated with endometriosis has a multifold etiology in spontaneous and induced disease.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Endometriosis Estrogens Gene Expression Regulation Oncogene Proteins v-fos Animals Chemokine CCL11 Chemokines, CC Chemokines, CC Disease Models, Animal Endometriosis Endometriosis Estrogens Female Infertility, Female Infertility, Female Oligonucleotide Array Sequence Analysis Oncogene Proteins v-fos Oncogene Proteins v-fos Papio

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