The role of eosinophil receptors in the non-genomic response to oestrogens in the uterus

Abstract

Three independent groups of parameters of oestrogen stimulation in the rat uterus are mediated by three independent mechanisms of oestrogen action. The genomic response to oestrogens (increase in RNA and protein content) is mediated by the cytosol-nuclear receptor system. This response is suppressed by Actinomycin d. The cytosol-nuclear receptors have a higher affinity for oestradiol than for oestriol, therefore oestradiol is the more potent oestrogen for the genomic response to oestrogens. Any condition interfering with oestrogen binding by this system, or with cytosol oestrogen-receptor complex transfer to the nucleus, interferes with the genomic response to oestrogens. Oestrogen-induced uterine oedema, increase in vascular permeability, release of histamine, uterine eosinophilia and some other parameters of oestrogen stimulation are mediated by the eosinophil oestrogen receptor system. This response is not blocked by Actinomycin d. Therefore it is a non-genomic response. The eosinophil receptors have a higher affinity for oestriol than for oestradiol. Therefore oestriol is the stronger oestrogen for the response mediated by eosinophils. Any agent or condition interfering with migration of eosinophils to the uterus, e.g. cortisol, colchicine, blood eosinopenia of young animals, selectively blocks eosinophil-mediated response to oestrogens, but does not interfere with other oestrogenic responses. We propose a mechanism for eosinophil migration to the uterus and for the role of eosinophils in oestrogen action. Cyclic AMP is involved in a third mechanism of oestrogen action upon a separate group of parameters.