ID 110703
著者
Chen, Gang Department of Human Genetics and Public Health, Graduate School of Proteomics, Faculty of Medicine, The University of Tokushima|Core Research for Evolutional Science and Technology (CREST)
新家, 利一 Department of Human Genetics and Public Health, Graduate School of Proteomics, Faculty of Medicine, The University of Tokushima|Core Research for Evolutional Science and Technology (CREST)
キノシタ, ケイゴ Department of Human Genetics and Public Health, Graduate School of Proteomics, Faculty of Medicine, The University of Tokushima|Core Research for Evolutional Science and Technology (CREST)
Yan, Hong-Tao Department of Human Genetics and Public Health, Graduate School of Proteomics, Faculty of Medicine, The University of Tokushima|Core Research for Evolutional Science and Technology (CREST)
イワモト, テルアキ Department of Urology, St.Marianna Medical University School of Medicine|Core Research for Evolutional Science and Technology (CREST)
中堀, 豊 Department of Human Genetics and Public Health, Graduate School of Proteomics, Faculty of Medicine, The University of Tokushima|Core Research for Evolutional Science and Technology (CREST)
キーワード
sex differentiation
MIS
promoter
estrogen
estrogen receptor
資料タイプ
学術雑誌論文
抄録
Sex differentiation consists of multi-step pathway that involves expression of many different genes. Müllerian duct inhibitory substance (MIS) has a key role for regression of the Müllerian duct during male sex differentiation. Recently, endocrine disruptors (EDs), which often have estrogen-like activities, have caused concern over worldwide. It has been reported that estrogen regulates the MIS expression. Therefore, we tested whether ERαand ERβinfluence the MIS promoter activity in the NT2/D1 cell line which expresses many sex differentiation related genes such as SRY, SOX9, and DAX-1. RT-PCR analysis revealed that the NT2/D1 cells express bother ERβ in addition to MIS. Under the low concentration of 17β-estradiol (E2), the over-expression of exogenous ERα increased the MIS promoter activity 3.3-fold compared with the control. However, as E2 concentration was increased, the MIS promoter activity was decreased. For ERβ, we could not observe alterations of the MIS promoter activity. Furthermore, the over-expression of the exogenous SF-1 inhibited the activation of the MIS promoter with ERα. Although it remains unclear whether the effects of ERαon the MIS promoter are mediated through the genomic or the no-genomic actions, the present results suggest that ERα upregulates the MIS promoter activity in the NT2/D1 cells under low concentrations of E2, and that the two ERs may work in different manners for the MIS promoter activation. The present findings may be useful to understand the molecular mechanisms by which EDs or estrogens affect the MIS expression.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
50
3-4
開始ページ
192
終了ページ
198
並び順
192
発行日
2003
EDB ID
134486
フルテキストファイル
言語
eng
著者版フラグ
出版社版