Oestrogen receptor (ER)-alpha and ER-beta isoforms in normal endometrial and endometriosis-derived stromal cells

Mol Hum Reprod. 1999 Jul;5(7):651-5. doi: 10.1093/molehr/5.7.651.

Abstract

Several investigators have noted that hormone-dependent development of endometriosis implants lags behind that of simultaneously analysed eutopic endometrium. With the recent discovery of the oestrogen receptor-beta (ER-beta) isoform, the aim of this study was to investigate whether differences in the expression of ER-alpha and ER-beta might explain this observation. mRNA transcripts from endometrial stromal cells isolated from normal endometrium (NE) and from endometriomas (EI) were analysed using a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) technique. RT-PCR and Southern blot analyses of the two ER isoforms indicated that NE and EI stromal cells predominantly express ER-alpha mRNA, however the relative concentrations of ER isoform mRNA transcripts differed between the two cell types. Steady-state ER-alpha:ER-beta mRNA ratios were 15.5 +/- 2.8 and 5.2 +/- 0.9 respectively for NE and EI cells (P = 0.02). NE and EI stromal cells expressed ER proteins with similar Kd ( approximately 0.9 nM) and densities ( approximately 24 500 binding sites/cell) respectively. Functional ER expression was indicated by an increase in progesterone receptor concentrations of approximately 60% (P = 0.03) after incubation with 10 nM oestradiol. We postulate that differential transcript processing, ligand specificity and biological actions of the ER-alpha and -beta isoforms may influence differential growth responses in normal and ectopic endometrium.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Endometriosis / metabolism*
  • Endometriosis / pathology
  • Endometrium / cytology
  • Endometrium / metabolism*
  • Endometrium / pathology
  • Estradiol / pharmacology
  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Female
  • Humans
  • Protein Isoforms / genetics*
  • RNA, Messenger / genetics
  • Receptors, Estrogen / genetics*
  • Receptors, Progesterone / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stromal Cells / cytology
  • Stromal Cells / metabolism*
  • Stromal Cells / pathology
  • Transcription, Genetic*
  • Up-Regulation / drug effects

Substances

  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Protein Isoforms
  • RNA, Messenger
  • Receptors, Estrogen
  • Receptors, Progesterone
  • Estradiol