| Literature DB >> 29920869 |
Momoko Kobayashi1, Kaya Watanabe1, Ritsuko Matsumura2, Nozomi Anayama1, Akio Miyamoto1, Hitoshi Miyazaki3, Koyomi Miyazaki4, Takashi Shimizu1, Makoto Akashi2.
Abstract
Circadian dysfunction perturbs the female reproductive cycle. In particular, mice lacking the clock gene Bmal1 show severe infertility, implying that BMAL1 plays roles in ovulation and luteinization. Here, we examined temporal changes in clock gene expression in the ovary and oviduct before and during gonadotropin-induced follicular growth, ovulation, and luteinization in sexually immature mice. While the oviduct did not show a drastic change in clock gene expression, Bmal1 expression in the ovary was higher than that in control mice during the period from 4 to 16 hr after human chorionic gonadotropin (hCG) administration. Bmal1 expression reached a maximum at 16 hr after hCG administration, when follicle luteinization occurred. In an interesting manner, administration of hCG to ex vivo-cultured oviduct triggered a shorter circadian period and inevitably resulted in phase advance. Together, our present data suggest that LH surge induces continuous expression of BMAL1 in the mouse ovary and modulates circadian phase in the mouse oviduct.Entities:
Keywords: circadian rhythm; clock gene; luteinizing hormone; ovary; oviduct
Year: 2018 PMID: 29920869 DOI: 10.1111/gtc.12605
Source DB: PubMed Journal: Genes Cells ISSN: 1356-9597 Impact factor: 1.891