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Estrogen induces the expression of estrogen receptor in human macrophages
Author(s) -
Jensen Amy L,
Pioli Patricia A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.672.43
Subject(s) - estrogen receptor , estrogen , endocrinology , medicine , monocyte , estrogen receptor alpha , messenger rna , immune system , receptor , biology , chemistry , microbiology and biotechnology , immunology , gene , biochemistry , cancer , breast cancer
Monocytes and macrophages (Mφs) are exposed to fluctuations in estradiol (E2) during the menstrual cycle. In some cell types E2 has been shown to regulate expression of its own receptor (ER). E2 levels peak pre‐ovulation and during pregnancy when regulation of immune responses is needed to ensure reproductive success. We hypothesized that E2 up‐regulates ER expression to increase sensitivity to E2 and subsequently influence E2‐regulated inflammatory responses. As human monocytes and Mφs express both isoforms of the ER, ERα and ERβ, we determined whether E2 influences ER expression in these cells. We found no gender difference in mRNA or protein levels in monocytes and MØs. E2 treatment augmented ERα mRNA and protein expression in female Mφs and this was at least in part mediated transcriptionally. Intriguingly, E2 had no effect on monocyte ERα mRNA and protein levels. Up‐regulation of ERα during monocyte‐to‐Mφ differentiation correlated with an increased inhibitory effect of E2 on LPS‐induced IL‐8 production. These data show that ERα is differentially expressed and regulated in human monocytes and Mφs, and E2 acts as a positive regulator of ERα in Mφs. Importantly, ERα expression correlates with the ability of E2 to influence Mφ activation. This may be important when E2 levels are high and tolerance of sperm and an allogeneic fetus are imperative. Supported by NIH AI51877 and NIH T32AR007576 (to ALJ)