Clinical Immunology· 2014Q2
Immunomodulation by the estrogen metabolite 2-methoxyestradiol
- 13citations
- Q2SCImago
- 2014year
Short summary
The estrogen metabolite 2-methoxyestradiol (2me2) selectively increases NK and T-cells in mice at low doses (2me2L), while higher doses (2me2H) mimic estrogen's effects on uterus proliferation and ERE activation.
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Key points
- Low-dose 2-methoxyestradiol (2me2L) increased NK and T-cells in bone marrow, spleen, and liver of mice.
- High-dose 2me2 (2me2H) and estradiol (E2) induced uterus proliferation in ovariectomized mice.
- Both 2me2H and E2 activated estrogen response elements (EREs).
- Estradiol (E2) demonstrated more potent immune regulation than 2me2.
AI-generated from the title and abstract; the full text is not read.
Abstract
2-methoxyestradiol (2me2), a metabolite of 17β-estradiol (E2), has been tested in phase II clinical cancer trials and models of inflammation. Its effects are only partly clarified. We investigated the effects of 2me2 on the immune system, using ovariectomized or sham-operated mice treated with a high and a low dose of 2me2 (2me2H and 2me2L), E2 or vehicle. We investigated antagonism of tissue proliferation and estrogen response element (ERE) activation. Established immunomodulation by E2 was reproduced. 2me2L increased NK and T-cells from bone marrow, spleen and liver. Both 2me2H and E2 induced uterus proliferation in ovariectomized mice, but no antagonistic effects on uteri growth were seen in intact animals. Both E2 and 2me2H activated EREs. Immunomodulation by 2me2 is tissue-, and concentration dependent. E2 regulated the immune system more potently. The higher dose of 2me2 resulted in E2 like effects, important to consider when developing 2me2 as a drug.
The authors' abstract, as published at the source. Clinical Immunology, 2014 · DOI ↗
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Field: Genetics (Biochemistry, Genetics and Molecular Biology)
GeneticsBiochemistry, Genetics and Molecular Biology