Retinoic acid has the potential to suppress endometriosis development

J Ovarian Res. 2015 Jul 31:8:49. doi: 10.1186/s13048-015-0179-6.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Proliferation / drug effects*
  • Endometriosis / drug therapy*
  • Endometriosis / genetics
  • Endometriosis / pathology
  • Estradiol / genetics
  • Estradiol Dehydrogenases / biosynthesis*
  • Estradiol Dehydrogenases / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • RNA, Messenger / biosynthesis
  • Stromal Cells / drug effects
  • Stromal Cells / pathology
  • Transcriptome / genetics
  • Tretinoin / administration & dosage*

Substances

  • RNA, Messenger
  • Estradiol
  • Tretinoin
  • Estradiol Dehydrogenases
  • HSD17B2 protein, human