Roles of estrogen receptor α (ERα) in the regulation of the human Müllerian inhibitory substance (MIS) promoter Roles of estrogen receptor α (ER α ) in the regulation of the human Mullerian inhibitory substance (MIS) promoter

Access this Article

Search this Article

Author(s)

    • Chen Gang
    • 徳島大学医学部 Published by The University of Tokushima School of Medicine
    • Shinka Toshikatsu
    • 徳島大学医学部 Published by The University of Tokushima School of Medicine
    • Kinoshita Keigo
    • 徳島大学医学部 Published by The University of Tokushima School of Medicine

Abstract

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.

Journal

  • The journal of medical investigation : JMI

    The journal of medical investigation : JMI 50(3-4), 192-198, 2003

    The University of Tokushima

Codes

  • NII Article ID (NAID)
    110002238351
  • NII NACSIS-CAT ID (NCID)
    AA11166929
  • Text Lang
    ENG
  • Article Type
    journal article
  • ISSN
    1343-1420
  • Data Source
    NII-ELS  IR 
Page Top