Changes in Eutopic Endometrial Gene Expression During the Progression of Experimental Endometriosis in the Baboon, Papio Anubis1

Yalda Afshar, Julie Hastings, Julie M. Hastings, Damian Roqueiro, Jae‐Wook Jeong, Jae-Wook Jeong, Linda C Giudice, Asgerally T Fazleabas
Biology of reproduction · 2013 · vol. 88(2) , pp. 44 · doi:10.1095/biolreprod.112.104497 · PMID:23284138 · W2141020709
article OA: bronze CC0 ⤵ 62 in-corpus citations
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This study in baboons demonstrates that the development of endometriosis directly alters eutopic endometrial gene expression, causing early dysregulation of signaling pathways and eventually a progesterone-resistant phenotype similar to human disease.

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Abstract

Endometriosis is associated with aberrant gene expression in the eutopic endometrium of women with disease. To determine if the development of endometriotic lesions directly impacts eutopic endometrial gene expression, we sequentially analyzed the eutopic endometrium across the time course of disease progression in a baboon model of induced disease. Endometriosis was induced in baboons (n = 4) by intraperitoneal inoculation of autologous menstrual endometrium. Eutopic endometria were collected during the midsecretory phase (Days 9-11 postovulation) at 1, 3, 6-7, 10-12, and 15-16 mo after disease induction and compared with tissue from disease-free baboons. RNA was hybridized to Human Genome U133 Plus 2.0 Arrays, and data were extracted using Gene-Chip Operating Software. Subsequently, both Gene Set Enrichment Analysis and Ingenuity Pathways Analysis were used to find biological states that have a statistically significant enrichment concomitant with pairwise comparison of human endometriosis arrays. Within 1 mo of induction of the disease, 4331 genes were differentially expressed (P < 0.05). Hierarchical clustering revealed self-segregation into two groups-a) 1, 3, and 10-12 mo and b) 6-7 and 15-16 mo-together with controls. Clustering analysis at each stage of disease validated dysregulation of several signaling pathways, including Nodal-like receptor, EGF, ERK/MAPK, and PI3/AKT. Sequential analysis of the same animals during disease progression demonstrated an early disease insult and a transitory dominance of an estrogenic phenotype; however, as the disease progressed, a progesterone-resistant phenotype became evident. Furthermore, we demonstrate a 38.6% differential gene expression overlap with endometrial samples in the midsecretory phase from women with endometriosis, concomitant with similar dysregulation in human disease candidate genes Fos, Nodal, Suclg2, and Kras, among others. Molecular changes in the eutopic endometrium, associated with endometriosis, are directly impacted by endometriotic lesions, providing strong evidence that it is the disease rather than inherent defective endometrium that results in aberrant gene expression in the eutopic endometrium. Furthermore, this baboon model provides a powerful means whereby the early events associated with the pathology of disease and the resulting infertility may be elucidated.

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Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Disease Progression Endometriosis Endometrium Gene Expression Regulation Papio anubis Signal Transduction Animals Disease Models, Animal Endometriosis Endometriosis Endometrium Epidermal Growth Factor Epidermal Growth Factor Epidermal Growth Factor Extracellular Signal-Regulated MAP Kinases Extracellular Signal-Regulated MAP Kinases Extracellular Signal-Regulated MAP Kinases Female Gene Expression Regulation Gene Expression Regulation

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