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Am J Reprod Immunol. 2018 Jan;79(1). doi: 10.1111/aji.12781. Epub 2017 Nov 6.

Medroxyprogesterone acetate-treated human, primary endometrial epithelial cells reveal unique gene expression signature linked to innate immunity and HIV-1 susceptibility.

Author information

1
Department of Pathology and Molecular Medicine, Michael G. DeGroote Center for Learning and Discovery, McMaster University, Hamilton, ON, Canada.
2
McMaster Immunology Research Center, Michael G. DeGroote Center for Learning and Discovery, McMaster University, Hamilton, ON, Canada.
3
McMaster Institute for Research on Aging, McMaster Innovation Park, McMaster University, Hamilton, ON, Canada.

Abstract

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 (GECs) 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 GECs 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 GECs 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 GECs and allows us to posit possible mechanisms of the MPA-mediated increase in HIV-1 acquisition.

KEYWORDS:

HIV-1; endometrium; estradiol; medroxyprogesterone acetate; progesterone; transcriptome

PMID:
29105931
DOI:
10.1111/aji.12781
[Indexed for MEDLINE]

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