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Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein.

Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Research Abstract Details 

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  • Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Abstract Text:

    qiyuan liuQiyuan Liu,kathleen a merklerKathleen A Merkler,xiaohui zhangXiaohui Zhang,mark p mcleanMark P McLean,

    Prostaglandin F2alpha (PGF2alpha) plays a pivotal role in ovarian luteolysis by inhibiting the expression of steroidogenic acute regulatory (StAR) protein, leading to a decrease in intracellular cholesterol transport and luteal steroid production. Previously we have demonstrated that the transcription factor Yin Yang 1 (YY1) bound to three regions in the StAR promoter in vitro and repressed promoter activity. This study further defined the YY1-mediated PGF2alpha effect on the inhibition of StAR protein expression through YY1 interaction with a single region in the StAR promoter in vivo. PGF2alpha consistently suppressed StAR mRNA and protein expression in cultured luteal cells in a dose-dependent manner. PGF2alpha also enhanced YY1 protein expression and binding to its cis-element in a time-dependent pattern that preceded the decline in StAR protein levels. The StAR promoter region bound by YY1 was also associated with histone deacetylase 1 (HDAC1). PGF2alpha treatment promoted HDAC1 binding to and suppressed the histone H3 acetylation in this region. On the contrary, YY1 knockdown decreased HDAC1 binding, increased histone H3 acetylation, enhanced StAR protein expression, and negated PGF2alpha effect on StAR protein expression. Luciferase assays showed that YY1 overexpression inhibited StAR promoter activity and the addition of a HDAC inhibitor, trichostatin A, abrogated the effect of YY1. Trichostatin A-treated luteal cells displayed increased StAR protein expression. These data indicate that PGF2alpha enhances a direct YY1/StAR promoter interaction and the recruitment of HDAC1 to the promoter, thereby preventing transcriptional activation of the StAR gene.

    Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Publishing Authors By Initials

    q liuQ Liu,ka merklerKA Merkler,x zhangX Zhang,mp mcleanMP McLean,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

    MEDLINE DATE:

    Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Endocrinology

    VOLUME: 148

    Page Numbers: 5209-19

    Journal Abbreviation: Endocrinology

    ISSN: 0013-7227

    DAY: 16

    MONTH: 08

    YEAR: 2007

    Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Information

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    LANGUAGE: eng

    NlmUniqueID: 375040

    Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Keywords Mesh Terms:

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    Chemical & Substance for Abstract: Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein. Information

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    Grant and Affiliation Information for Prostaglandin F2alpha suppresses rat steroidogenic acute regulatory protein expression via induction of Yin Yang 1 protein and recruitment of histone deacetylase 1 protein.

    AFFILIATION: Department of Obstetrics and Gynecology, University of South Florida, Tampa, FL 33612, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NICHD

    GRANT: HD35163

    ACRONYM: HD

    MEDLINETA: Endocrinology

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