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• W1998802005 abstract "RATIONALE: A role for female hormones in the increased prevalence of asthma in women has been suggested. We have reported that estradiol (E2) potentiates the release of allergic mediators from a rat mast cell line. To define the role of classic ERs in this effect, we examined the expression and role of these receptors in BMMCs from wild-type (WT) and ERα knockout (KO) mice.METHODS: The expression of ERα and β were assessed by RT-PCR. The effects of E2 ± a nominal allergen (DNP-BSA) on degranulation was assessed by β-hexosaminidase release, expressed as the mean+SE of the percentage of the total cellular content.RESULTS: BMMCs of WT mice expressed mRNA for ERα, but not ERβ. E2 (100 pM) induced release of β-hexosaminidase from WT BMMCs (7.5+1.5 %), but not from the ERα KO. IgE-dependent release from WT BMMCs (3.5+1.0 %) increased (6.1+1.0 %) in the presence of 10 pM of E2 (p<0.05).CONCLUSIONS: These results indicate that BMMCs, like rat mast cell lines, express ERα. Exposure to physiological doses of E2 induce the release of a substantial portion of their preformed mediators and augmented IgE-dependent release. The lack of E2-mediated release of β- hexosaminidase from ERα KO BMMCs suggests that ERα is required for this activity. This finding may help to identify new approaches for treating women with asthma. RATIONALE: A role for female hormones in the increased prevalence of asthma in women has been suggested. We have reported that estradiol (E2) potentiates the release of allergic mediators from a rat mast cell line. To define the role of classic ERs in this effect, we examined the expression and role of these receptors in BMMCs from wild-type (WT) and ERα knockout (KO) mice. METHODS: The expression of ERα and β were assessed by RT-PCR. The effects of E2 ± a nominal allergen (DNP-BSA) on degranulation was assessed by β-hexosaminidase release, expressed as the mean+SE of the percentage of the total cellular content. RESULTS: BMMCs of WT mice expressed mRNA for ERα, but not ERβ. E2 (100 pM) induced release of β-hexosaminidase from WT BMMCs (7.5+1.5 %), but not from the ERα KO. IgE-dependent release from WT BMMCs (3.5+1.0 %) increased (6.1+1.0 %) in the presence of 10 pM of E2 (p<0.05). CONCLUSIONS: These results indicate that BMMCs, like rat mast cell lines, express ERα. Exposure to physiological doses of E2 induce the release of a substantial portion of their preformed mediators and augmented IgE-dependent release. The lack of E2-mediated release of β- hexosaminidase from ERα KO BMMCs suggests that ERα is required for this activity. This finding may help to identify new approaches for treating women with asthma." @default.
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• W1998802005 date "2006-02-01" @default.
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• W1998802005 title "Estradiol Enhances the Release of Allergic Mediator from Bone Marrow-derived Mast Cells (BMMCs) Via Estrogen Receptor α (ERα)" @default.
• W1998802005 doi "https://doi.org/10.1016/j.jaci.2005.12.260" @default.
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