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Medroxyprogesterone acetate‐treated human, primary endometrial epithelial cells reveal unique gene expression signature linked to innate immunity and HIV ‐1 susceptibility
Author(s) -
Woods Matthew W.,
Zahoor Muhammad Atif,
Dizzell Sara,
Verschoor Chris P.,
Kaushic Charu
Publication year - 2018
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12781
Subject(s) - medroxyprogesterone acetate , innate immune system , gene expression , biology , progestin , estrogen , microarray analysis techniques , immunology , hormone , endometrium , progestogen , immunity , gene , endocrinology , medicine , immune system , genetics
Problem Medroxyprogesterone acetate ( MPA ), a progestin‐based hormonal contraceptive designed to mimic progesterone, has been linked to increased human immunodeficiency virus ( HIV ‐1) susceptibility. Genital epithelial cells ( GEC s) form the mucosal lining of the female genital tract ( FGT ) and provide the first line of protection against HIV ‐1. The impact of endogenous sex hormones or MPA on the gene expression profile of GEC s has not been comprehensively documented. Method of study Using microarray analysis, we characterized the transcriptional profile of primary endometrial epithelial cells grown in physiological levels of E2, P4, and MPA . Results Each hormone treatment altered the gene expression profile of GEC s in a unique manner. Interestingly, although MPA is a progestogen, the gene expression profile induced by it was distinct from P4. MPA increased gene expression of genes related to inflammation and cholesterol synthesis linked to innate immunity and HIV ‐1 susceptibility. Conclusion The analysis of gene expression profiles provides insights into the effects of sex hormones and MPA on GEC s and allows us to posit possible mechanisms of the MPA ‐mediated increase in HIV ‐1 acquisition.