Retinoic acid has the potential to suppress endometriosis development

Yoshiaki Yamagata, Eiichi Takaki, Masahiro Shinagawa, Maki Okada, Kosuke Jozaki, Lifa Lee, Shun Sato, Ryo Maekawa, Toshiaki Taketani, Hiromi Asada, Hiroshi Tamura, Akira Nakai, Norihiro Sugino
Journal of ovarian research · 2015 · vol. 8(1) , pp. 49 · doi:10.1186/s13048-015-0179-6 · PMID:26228249 · W1905020050
article OA: gold CC0 ⤵ 20 in-corpus citations
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Abstract

BACKGROUND: Despite endometriosis is common estrogen dependent disease afflicting women in reproductive age, the pathogenesis has not been fully elucidated. Retinoic acid has various functions in cells as biologic modulator, and aberrant retinoid metabolism seems to be involved in the lesions of endometriosis. In order to evaluate the potential of all-trans retinoic acid (ATRA) for therapeutic treatment, a transcriptome analysis and estradiol measurements in cultured endometriotic cells and tissues were conducted. METHODS: The mRNA expression levels in ATRA-treated endometriotic stromal cells (ESC) isolated from ovarian endometrial cysts (OEC) were investigated. Estradiol production in OEC tissues was also investigated. RESULTS: In the isolated ESC culture supplemented with ATRA for four days, total RNA was extracted followed by a transcriptome analysis using GeneChip. Forty-nine genes were upregulated and four genes were down-regulated by the ATRA treatment. Many upregulated genes were associated with the negative regulation of cellular proliferation. In addition, ATRA treatment decreased the mRNA expression of 17-beta-dehydrogenase 2 (HSD17B2) which converts estradiol into estrone in a dose-dependent manner, and the ELISA measurements indicated that estradiol production in the OEC tissue was inhibited by ATRA treatment. CONCLUSIONS: Retinoic acid has the potential to suppress endometriosis development.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Cell Proliferation Endometriosis Estradiol Dehydrogenases Tretinoin Adult Cell Proliferation Endometriosis Endometriosis Endometriosis Estradiol Estradiol Estradiol Dehydrogenases Estradiol Dehydrogenases Female Gene Expression Regulation, Neoplastic Gene Expression Regulation, Neoplastic Humans RNA, Messenger RNA, Messenger Stromal Cells

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