Search Results

You are looking at 1 - 2 of 2 items for

  • Author: Hirotaka Nishi x
  • Refine by access: All content x
Clear All Modify Search
Kazuhiro Tamura Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Kazuhiro Tamura in
Google Scholar
PubMed
Close
,
Mikihiro Yoshie Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Mikihiro Yoshie in
Google Scholar
PubMed
Close
,
Hirotaka Nishi Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Hirotaka Nishi in
Google Scholar
PubMed
Close
,
Yumi Osakabe Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Yumi Osakabe in
Google Scholar
PubMed
Close
,
Keiichi Isaka Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Keiichi Isaka in
Google Scholar
PubMed
Close
,
Takahiko Hara Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Takahiko Hara in
Google Scholar
PubMed
Close
, and
Hiroshi Kogo Department of Endocrine Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1, Horinouch, Hachioji, Tokyo 192-0392, Japan, Department of Obstetrics and Gynecology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan and Stem Cell Project Group, The Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan

Search for other papers by Hiroshi Kogo in
Google Scholar
PubMed
Close

The cytosolic phosphoprotein stathmin is upregulated at the site of embryo implantation in the rodents. However, stathmin expression in the human uterus has not yet been investigated. The distribution of uterine and placental stathmin was analyzed by immunohistochemistry, while stathmin mRNA expression was detected in endometrial tissues by the reverse transcriptase-PCR. Cultured endometrial stromal cells were used to investigate whether stathmin plays a role in decidualization. Stathmin is expressed specifically in the glandular epithelium and the stromal cells of human endometrial tissue. It is also expressed by cytotrophoblasts and extravillous trophoblasts, but not by syncytiotrophoblasts or decidual tissues during the first trimester of pregnancy. When stromal cells isolated from normal endometrial tissues were cultured and stimulated to decidualize by progesterone (P4) plus estrogen or dibutyryl cyclic 3′,5′-AMP, their total and phosphorylated stathmin levels decreased. Knocking down stathmin expression in the cultured stromal cells using small interfering RNA, before the cells were exposed to the decidualizing agents, significantly suppressed decidualization, as indicated by the decreased expression of IGF-binding protein-1 and prolactin. Stathmin is differently expressed in human endometrial and placental cells and may participate in the decidualization of endometrial stromal cells.

Free access
Tomomi Kawamura Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Tomomi Kawamura in
Google Scholar
PubMed
Close
,
Yidan Dai Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Yidan Dai in
Google Scholar
PubMed
Close
,
Masanori Ono Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Masanori Ono in
Google Scholar
PubMed
Close
,
Takayuki Kikuchi Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Takayuki Kikuchi in
Google Scholar
PubMed
Close
,
Akina Yamanaka Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Akina Yamanaka in
Google Scholar
PubMed
Close
,
Keiko Ueno Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Keiko Ueno in
Google Scholar
PubMed
Close
,
Junya Kojima Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Junya Kojima in
Google Scholar
PubMed
Close
,
Tomoko Fujiwara Department of Social Work and Life Design, Kyoto Notre Dame University, Kyoto, Japan

Search for other papers by Tomoko Fujiwara in
Google Scholar
PubMed
Close
,
Takiko Daikoku Division of Animal Disease Model, Research Center for Experimental Modeling of Human Disease, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan

Search for other papers by Takiko Daikoku in
Google Scholar
PubMed
Close
,
Yoshiko Maida Department of Nursing, College of Medical, Pharmaceutical, and Health Sciences, Kanazawa University, Kanazawa, Japan

Search for other papers by Yoshiko Maida in
Google Scholar
PubMed
Close
,
Hitoshi Ando Department of Cellular and Molecular Function Analysis, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan

Search for other papers by Hitoshi Ando in
Google Scholar
PubMed
Close
,
Hiroshi Fujiwara Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan

Search for other papers by Hiroshi Fujiwara in
Google Scholar
PubMed
Close
,
Naoaki Kuji Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Naoaki Kuji in
Google Scholar
PubMed
Close
, and
Hirotaka Nishi Department of Obstetrics and Gynecology, Tokyo Medical University, Tokyo, Japan

Search for other papers by Hirotaka Nishi in
Google Scholar
PubMed
Close

In brief

In this study, we examined the relationship between BMAL1 expression and the genes regulating steroid biosynthesis in human luteinized granulosa cells. BMAL1 function is crucial for steroid production and proper ovarian function, highlighting the importance of circadian clock regulation in female reproductive health.

Abstract

Human luteinized granulosa cells were collected to analyze circadian clock gene expression and its effect on the genes regulating steroid biosynthesis. We used siRNA to knock down the expression of BMAL1 in KGN cells. We measured the expression levels of genes regulating steroid biosynthesis and circadian clock RT-qPCR. We demonstrated that BMAL1 expression positively correlates with genes regulating steroid biosynthesis (CYP11A1, CYP19A1, STAR, and ESR2). The knockdown of BMAL1 in KGN cells revealed a significant decrease in steroid synthase expression. In contrast, when BMAL1 was overexpressed in KGN and HGL5 cells, we observed a significant increase in the expression of steroid synthases, such as CYP11A1 and CYP19A1. These results indicated that BMAL1 positively controls 17β-estradiol (E2) secretion in granulosa cells. We also demonstrated that dexamethasone synchronization in KGN cells enhanced the rhythmic alterations in circadian clock genes. Our study suggests that BMAL1 plays a critical role in steroid biosynthesis in human luteinized granulosa cells, thereby emphasizing the importance of BMAL1 in the regulation of reproductive physiology.

Restricted access