Abstract

The transient potential receptor (TRP) channels are membrane-binding proteins that are non-selectively permeable for cations, such as Ca2+ and Mg2+, in numerous mammalian cells. The extracellular or intracellular ions play key roles in physiological function, including muscle contraction, cytokine production, insulin release, and apoptosis. Although TRPM channels have been implicated in the brain, bone marrow, and spleen, the presence of TRPM2 has been reported in the endometrium of the uterus. To determine whether expression of the TRPM2 gene in the uterus is due to gonadal steroid hormones or a hormone-independent effect, the uterine TRPM2 gene was monitored in mature rats during the oestrous cycle and in immature rats after treatment with gonadal steroid oestrogen (E2), progesterone (P4) with/without their antagonist, ICI 182,780, and RU486. Dramatic induction of the level of TRPM2 mRNA occurs at proestrus, followed by a drop to baseline levels at metestrus, and its level is restored at diestrus. Furthermore, the immune-reactive TRPM2 is observed in stromal cells of the myometrium and endometrium, and changes during the oestrus cycle. In addition, E2-induced TRPM2 is inhibited by co-treatment with P4. Taken together, these results imply that TRPM2 expression levels in the uterus are regulated by gonadal steroid hormones E2 and P4. Results of this study suggest possible involvement of TRPM2 in reproductive function during the oestrous cycle in female rats.

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