ArticleMolecular and cellular biochemistry2004
17-Beta estradiol enhances prostaglandin E2 production in human U937-derived macrophages.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 15 citations in OpenAlex.
- Regulation of Stromal Cells by Sex Steroid Hormones in the Breast Cancer Microenvironment.Cancers · 2024Review
- Premenopausal and postmenopausal women during the COVID-19 pandemic.Przeglad menopauzalny = Menopause review · 2022Review
- Immune Tumor Microenvironment in Breast Cancer and the Participation of Estrogen and Its Receptors in Cancer Physiopathology.Frontiers in immunology · 2019Review
- Significant increase of prostaglandin E-major urinary metabolite in male smokers: a screening study of age and gender differences using a simple radioimmunoassay.Journal of clinical laboratory analysis · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandins (PGs) are potent eicosanoid lipid mediators that have been implicated in numerous homeostatic functions and inflammation. Estrogens have been shown to regulate the expression of genes in lipid metabolism in many cellular systems. In this study, the activation of macrophages and the modulation of PG release by estrogens were examined. The effects of 17-alpha and 17-beta estradiols, phytoestrogen Genistein and several selective estrogen receptor modulators on the release of PGE2 were investigated in human U937-derived macrophages. 17-Beta estradiol caused an enhancement of PGE2 production in a time- and dose-dependent manner. Treatment of macrophages with 17-beta estradiol elicited an increased arachidonic acid (AA) release and an up-regulation of both cyclooxygenesis-1 and cyclooxygenesis-2 enzymes at both the transcript and protein levels. In addition, immunostaining of nuclear estrogen receptor alpha and the observation of ICI182 780 blockade of PGE2 production indicated that 17-beta estradiol-induced PGE2 release was mainly through nuclear estrogen receptor alpha.
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Registered trials
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