Specific estrogen binding sites in human lymphoid cells and thymic cells

Danel, L.; Souweine, Gilbert; Monier, J. C.; Saez, S.

doi:10.1016/0022-4731(83)90131-0

Cited by 148 publications

(46 citation statements)

References 20 publications

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“…In addition, estrogen has been implicated in control of gene expression unrelated to sexual differentiation and reproduction (12,25,33). Activation of estrogen-responsive genes occurs via interaction of the estrogen receptor (ER) with 17-beta estradiol (E2) and subsequent receptor binding to estrogen-responsive elements (EREs) of target genes.…”

mentioning

confidence: 99%

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Segars¹,

Marks²,

Hirschfeld³

et al. 1993

Mol. Cell. Biol.

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The retinoid X receptor 13 (RXRI; H-2RIIBP) forms heterodimers with various nuclear hormone receptors and binds multiple hormone response elements, including the estrogen response element (ERE). In this report, we show that endogenous RXR3 contributes to ERE binding activity in nuclear extracts of the human breast cancer cell line MCF-7. To define a possible regulatory role of RXRf3 regarding estrogen-responsive transcription in breast cancer cells, RXRI3 and a reporter gene driven by the vitellogenin A2 ERE were transfected into estrogen-treated MCF-7 cells. RXR13 inhibited ERE-driven reporter activity in a dosedependent and element-specific fashion. This inhibition occurred in the absence of the RXR ligand 9-cis retinoic acid. The RXRB-induced inhibition was specific for estrogen receptor (ER)-mediated ERE activation because inhibition was observed in ER-negative MDA-MB-231 cells only following transfection of the estrogen-activated ER. No inhibition of the basal reporter activity was observed. The inhibition was not caused by simple competition of RXRI3 with the ER for ERE binding, since deletion mutants retaining DNA binding activity but lacking the N-terminal or C-terminal domain failed to inhibit reporter activity. In addition, cross-linking studies indicated the presence of an auxiliary nuclear factor present in MCF-7 cells that contributed to RXRI3 binding of the ERE. Studies using known heterodimerization partners of RXR13 confirmed that RXRP/ triiodothyronine receptor ai heterodimers avidly bind the ERE but revealed the existence of another triiodothyronine-independent pathway of ERE inhibition. These results indicate that estrogen-responsive genes may be negatively regulated by RXRI3 through two distinct pathways.

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mentioning

confidence: 99%

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Segars¹,

Marks²,

Hirschfeld³

et al. 1993

Mol. Cell. Biol.

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“…This might be expected to reflect the in vivo situation more closely than could previously be accomplished. The presence of sex steroid receptors in these primary cells [43][44][45] has been demonstrated recently and is important in an examination of sex steroid modulation of lipoprotein metabolism. The use of AcLDL is well established as a standard form of modified lipoprotein in foam cell experiments, because it is specific for the scavenger receptor pathway for lipoprotein uptake.…”

Section: Discussionmentioning

confidence: 96%

Estrogen and Progesterone Reduce Lipid Accumulation in Human Monocyte-Derived Macrophages

et al. 1999

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Background-Males have an earlier onset and greater prevalence of clinical atherosclerosis than age-matched females, which is consistent with an atheroprotective effect of the female sex steroids, estrogen and progesterone. We therefore examined the effects of estrogen and progesterone on human foam cell formation, a key early event in atherogenesis. Methods and Results-Monocytes from healthy female and male donors were obtained from white cell concentrates and allowed to differentiate into macrophages over 10 days. These human monocyte-derived macrophages (MDMs) were exposed to either control (0.1% vol/vol ethanol) or estrogen or progesterone treatment on days 3 through 10. Lipid loading was achieved on days 8 through 10 by incubation with acetylated LDL. Lipid from the MDMs was then extracted for analysis of cholesteryl ester (CE) content. 17␤-Estradiol at both physiological (2 nmol/L) and supraphysiological (20 and 200 nmol/L) concentrations produced a significant reduction in macrophage CE content (88Ϯ3%, 88Ϯ2%, and 85Ϯ4%, respectively; PϽ0.02 compared with control). Physiological and supraphysiological levels of progesterone (2, 10, and 200 nmol/L) produced an even more dramatic reduction in CE content (74Ϯ9%, 56Ϯ10%, and 65Ϯ8%, respectively; PϽ0.002 compared with control). This effect could be abrogated by coincubation with the progesterone receptor antagonist RU486. Neither estrogen nor progesterone produced a reduction in lipid loading in male-donor-derived MDMs. Detailed lipid trafficking studies demonstrated that both estrogen and progesterone altered macrophage uptake and/or processing of modified LDL. Conclusions-Physiological levels of estrogen and progesterone are associated with a female-sex-specific reduction in human macrophage lipid loading, which is consistent with an atheroprotective effect. (Circulation. 1999;100:2319-2325.)

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“…Previous studies has also documented that male sex hormone, testosterone plays an important role for infections with parasitic protozoans inducing an immuno-suppressive effect (Greenblatt, 1980;Alexander, 1988). Macrophages and lymphocytes, the two major cell types involved in the disease outcome of leishmaniasis, possesses receptors for sex hormones such as androgen, estrogens and progesterone (Wunderlich et al, 2002;Danel et al, 1983;Jones et al, 2008). Based on these data it is not surprising that testosterone could affect the outcomes of VL.…”

Section: Ajimentioning

confidence: 84%

Association of Testosterone and Cholesterol Level in Modulation of Immunity and Severity of Disease in Visceral Leishmaniasis Patients-a Preliminary Study

Pandey¹

2014

American Journal of Immunology

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Males are more prone to Visceral Leishmaniasis (VL) as compared to females. The role of androgens in host defence against Leishmania and other pathogens is of considerable interest. This study was aimed to understand a baseline mechanistic understanding of the pathogenesis of visceral leishmaniasis with respect to testosterone. We examined the relationship between serum testosterone and cholesterol levels, antigen induced Interleukin-10 (IL-10) and Interferon-gamma (IFN-γ) and production by Peripheral Blood Mono Nuclear Cells (PBMCs) and parasite burden as determined by microscopic examination on male patients (n = 18) with VL and gender-and age-matched controls (n = 10). Testosterone plasma levels were found to be up regulated in VL patients as compared to healthy controls. In severely infected patients, the mean testosterone concentration was observed to be increased compared with other VL patients (p<0.001). Further, serum cholesterol level was found much down regulated during severe infection of VL (p<0.005) as compared to healthy control. Further an in-vitro stimulation of PBMCs of VL patients with exogenous testosterone resulted in an increase IL-10 production with a subsequent decline in host protective IFN-γ response. This study suggests that testosterone level might be linked to immuno-pathogenicity of VL infection. Whether testosterone level is probably a marker of severe VL infection with an immunosuppressive effect needs to be validated further.

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Specific estrogen binding sites in human lymphoid cells and thymic cells

Cited by 148 publications

References 20 publications

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Inhibition of estrogen-responsive gene activation by the retinoid X receptor beta: evidence for multiple inhibitory pathways.

Estrogen and Progesterone Reduce Lipid Accumulation in Human Monocyte-Derived Macrophages

Association of Testosterone and Cholesterol Level in Modulation of Immunity and Severity of Disease in Visceral Leishmaniasis Patients-a Preliminary Study

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