Eosinophil-mediated non-genomic parameters of estrogen stimulation--a separate group of responses mediated by an independent mechanism.
The present report describes evidence suggesting that eosinophil leukocytes mediate a separate group of responses to estrogens (uterine edema, increase in vascular permeability, release of histamine etc.) independently from genomic activation. Conditions suppressing genomic activation do not interfere with this group of responses. Conditions interfering with eosinophil leukocyte migration to the uterus (young age blood eosinopenia, eosinopenic hormones, agents blocking cell mobility) selectively interfere with this group of responses. It was proposed that estrogen cytosol-nuclear receptors are involved in estrogen-induced genomic activation, and that estrogen receptors from eosinophil leukocytes are involved in the migration of these cells to the uterus, where they would mediate the above responses. Conditions increasing (theophylline) or decreasing (thyroid hormones, insulin) estrogen binding by eosinophils selectively modify estrogen-induced uterine eosinophilia and the responses to estrogen proposed to be mediated by eosinophils in the uterus. A mechanism is proposed explaining estrogen effects mediated by eosinophils.
D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism; D000242:Cyclic AMP / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D004804:Eosinophils / Q000502:physiology*; D004967:Estrogens / Q000502:physiology*; D005260:Female; D008954:Models, Biological; D011453:Prostaglandins / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000502:physiology; D014599:Uterus / Q000502:physiology*
D004967:Estrogens; D011453:Prostaglandins; D011960:Receptors, Estrogen; D000242:Cyclic AMP