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Retinoic acid has the potential to suppress endometriosis development
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 end...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521362/ https://www.ncbi.nlm.nih.gov/pubmed/26228249 http://dx.doi.org/10.1186/s13048-015-0179-6 |
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author | Yamagata, Yoshiaki Takaki, Eiichi Shinagawa, Masahiro Okada, Maki Jozaki, Kosuke Lee, Lifa Sato, Shun Maekawa, Ryo Taketani, Toshiaki Asada, Hiromi Tamura, Hiroshi Nakai, Akira Sugino, Norihiro |
author_facet | Yamagata, Yoshiaki Takaki, Eiichi Shinagawa, Masahiro Okada, Maki Jozaki, Kosuke Lee, Lifa Sato, Shun Maekawa, Ryo Taketani, Toshiaki Asada, Hiromi Tamura, Hiroshi Nakai, Akira Sugino, Norihiro |
author_sort | Yamagata, Yoshiaki |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-4521362 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-45213622015-08-01 Retinoic acid has the potential to suppress endometriosis development Yamagata, Yoshiaki Takaki, Eiichi Shinagawa, Masahiro Okada, Maki Jozaki, Kosuke Lee, Lifa Sato, Shun Maekawa, Ryo Taketani, Toshiaki Asada, Hiromi Tamura, Hiroshi Nakai, Akira Sugino, Norihiro J Ovarian Res Research 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. BioMed Central 2015-07-31 /pmc/articles/PMC4521362/ /pubmed/26228249 http://dx.doi.org/10.1186/s13048-015-0179-6 Text en © Yamagata et al. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Yamagata, Yoshiaki Takaki, Eiichi Shinagawa, Masahiro Okada, Maki Jozaki, Kosuke Lee, Lifa Sato, Shun Maekawa, Ryo Taketani, Toshiaki Asada, Hiromi Tamura, Hiroshi Nakai, Akira Sugino, Norihiro Retinoic acid has the potential to suppress endometriosis development |
title | Retinoic acid has the potential to suppress endometriosis development |
title_full | Retinoic acid has the potential to suppress endometriosis development |
title_fullStr | Retinoic acid has the potential to suppress endometriosis development |
title_full_unstemmed | Retinoic acid has the potential to suppress endometriosis development |
title_short | Retinoic acid has the potential to suppress endometriosis development |
title_sort | retinoic acid has the potential to suppress endometriosis development |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521362/ https://www.ncbi.nlm.nih.gov/pubmed/26228249 http://dx.doi.org/10.1186/s13048-015-0179-6 |
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