Proteomic analysis of endometrium from fertile and infertile patients suggests a role for apolipoprotein A-I in embryo implantation failure and endometriosis

Jan J Brosens, Andrea Hodgetts, A. Hodgetts, Fahkera Feroze-Zaidi, F. Feroze-Zaidi, J Robert A Sherwin, J. R. A. Sherwin, Luca Fusi, L. Fusi, Madhuri S Salker, Jenny Higham, G. L. Rose, Gillian L Rose, T. Kajihara, Takeshi Kajihara, Steven L Young, B. A. Lessey, Bruce A Lessey, Patrick Henriet, Paul R Langford, A.T. Fazleabas, Asgerally T Fazleabas
Molecular human reproduction · 2009 · vol. 16(4) , pp. 273–285 · doi:10.1093/molehr/gap108 · PMID:20008415 · PMC2834406 · W2125005815
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Proteomic analysis identified apolipoprotein A-I as a potential factor in implantation failure, with altered expression and regulation observed in endometriosis patients and a primate model.

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Abstract

Pregnancy is dependent upon the endometrium acquiring a receptive phenotype that facilitates apposition, adhesion and invasion of a developmentally competent embryo. Surface-enhanced laser desorption/ionization time-of-flight mass spectrometry of mid-secretory endometrial biopsies revealed a 28 kDa protein peak that discriminated highly between samples obtained from women with recurrent implantation failure and fertile controls. Subsequent tandem mass spectroscopy unambiguously identified this peak as apolipoprotein A-I (apoA-I), a potent anti-inflammatory molecule. Total endometrial apoA-I levels were, however, comparable between the study and control group. Moreover, endometrial apoA-I mRNA expression was not cycle-dependent although there was partial loss of apoA-I immunoreactivity in luminal and glandular epithelium in mid-secretory compared with proliferative endometrial samples. Because of its putative anti-implantation properties, we examined whether endometrial apoA-I expression is regulated by embryonic signals. Human chorionic gonadotrophin (hCG) strongly inhibited apoA-I expression in differentiating explant cultures but not when established from eutopic endometrium from patients with endometriosis. Pelvic endometriosis was associated with elevated apoA-I mRNA levels, increased secretion by differentiating eutopic endometrial explant cultures and lack of hCG-dependent down-regulation. To corroborate these observations, we examined endometrial apoA-I expression and its regulation by hCG in a non-human primate model of endometriosis. As in humans, hCG strongly inhibited endometrial apoA-I mRNA expression in disease-free baboons, but this response was entirely lost upon induction of pelvic endometriosis. Together, these observations indicate that perturbations in endometrial apoA-I expression, modification or regulation by paracrine embryonic signals play a major role in implantation failure and infertility.

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Condition tags

endometriosisinfertility

MeSH descriptors

Apolipoprotein A-I Embryo Implantation Endometriosis Endometrium Infertility, Female Adult Animals Apolipoprotein A-I Blotting, Western Cells, Cultured Embryo Implantation Endometriosis Endometrium Enzyme-Linked Immunosorbent Assay Female Humans Immunohistochemistry Infertility, Female Mass Spectrometry Papio

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