Maintenance of uterine calcium balance is crucial for physiological functioning, including smooth muscle contraction and embryo implantation. Although calbindins were previously thought to act as important uterine calcium-processing genes for female reproductive function, they were not enough to attest the roles of calcium ions in the reproductive organs. Previously, we reported that rat transient receptor potential cation channel, subfamily V, member 6 (TRPV6) was expressed and regulated by hormones in the uterus. In the present study, we observed uterine TRPV6 expression in a mouse model to clarify the mutual roles of these two calcium-processing genes in female reproductive organs. We investigated uterine TRPV6 mRNA expression during the estrous cycle and pregnancy, as well as its regulation by the steroid hormones estrogen (E2) and progesterone (P4) in mice. Uterine TRPV6 mRNA levels increased at estrus and fluctuated in the uterus, placenta, and fetal membrane during pregnancy. Uterine TRPV6 mRNA increased in mid- and late pregnancy, and its expression was strongly induced in midpregnancy in the labyrinth and spongy zones of the placenta, and in the fetal membrane. E2 (17beta-estradiol) was found to regulate uterine TRPV6 expression in the luminal and glandular epitheliums. In addition, we determined that ERalpha tightly regulated uterine TRPV6 transcription. Together, these results suggest that for uterine function in normal pregnancy, TRPV6 is regulated by E2 via an ERalpha-dependent pathway.