ArticlePloS one2009
Estradiol regulates expression of estrogen receptor ERalpha46 in human macrophages.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
65 citing papers in PubMed, 130 citations in OpenAlex.
- Effect of menopausal hormone therapy on methylation levels in early and late postmenopausal women.Clinical epigenetics · 2022Trial
- Estradiol Enhances Alveolar Bone Resorption by Promoting Osteoclast Differentiation in Experimental Periodontitis.Dentistry journal · 2026Article
- Targeting estrogen receptor alpha in breast cancer for novel therapies resistance mechanisms and future directions.Discover oncology · 2025Review
- Transcriptome profiling of L. infantum-infected human macrophages reveals sex-specific type I interferon induction.PLoS pathogens · 2025Article
- The Estrogen-Immune Interface in Endometriosis.Cells · 2025Review
- Expression patterns of estrogen and androgen receptors in NSCLC patients according to the PD-L1 profile.Frontiers in immunology · 2025Article
- Regulation of Stromal Cells by Sex Steroid Hormones in the Breast Cancer Microenvironment.Cancers · 2024Review
- 17β-estradiol inhibits Notch1 activation in murine macrophage cell line RAW 264.7.Molecular biology reports · 2024Article
- Monocyte subsets in breast cancer patients under treatment with aromatase inhibitor and mucin-1 cancer vaccine.Journal of translational medicine · 2024Article
- Lower levels of the neuroprotective tryptophan metabolite, kynurenic acid, in users of estrogen contraceptives.Scientific reports · 2023Article
- 17α-estradiol, a lifespan-extending compound, attenuates liver fibrosis by modulating collagen turnover rates in male mice.American journal of physiology. Endocrinology and metabolism · 2023Article
- Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022Review
- Human monocytes respond to lipopolysaccharide (LPS) stimulation in a sex-dependent manner.Journal of cellular physiology · 2022Article
- Article
- Skeletal muscle wasting: the estrogen side of sexual dimorphism.American journal of physiology. Cell physiology · 2022Review
- Review
- Estrogen receptor-α signaling in post-natal mammary development and breast cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Estrogen Receptor Functions and Pathways at the Vascular Immune Interface.International journal of molecular sciences · 2021Review
- Expression of Estrogen Receptor α by Decidual Macrophages in Preeclampsia.Biomedicines · 2021Article
- Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundMonocytes and macrophages are key innate immune effector cells that produce cytokines and chemokines upon activation. We and others have shown that 17beta-estradiol (E2) has a direct role in the modulation of monocyte and macrophage immune function. However, relatively little is known about the ability of E2 to regulate isoform expression of estrogen receptors (ERs) in these cells. METHODOLOGY/PRINCIPAL
findingsIn this study, we quantify expression of ERalpha and ERbeta in human monocytes and macrophages. We also show for the first time that the N-terminal truncated ERalpha variant, ERalpha46, is expressed in both cell types. Promoter utilization studies reveal that transcription of ERalpha in both cell types occurs from upstream promoters E and F. Treatment with E2 induces ERalpha expression in macrophages but has no effect on ERbeta levels in either cell type. During monocyte-to-macrophage differentiation, ERalpha is upregulated in a time-dependent manner. Previous studies by our group demonstrated that E2 treatment attenuates production of the chemokine CXCL8 in an ER-dependent manner. We now show that ERalpha expression levels parallel the ability of E2 to suppress CXCL8 production. CONCLUSIONS/SIGNIFICANCE: This work demonstrates for the first time that human macrophages predominantly express the truncated ER variant ERalphap46, which is estradiol-inducible. This is mediated through usage of the ERalpha F promoter. Alternative promoter usage may account for tissue and cell type-specific differences in estradiol-induced effects on gene expression. These studies signify the importance of ERalpha expression and regulation in the ability of E2 to modulate innate immune responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.