Differential expression of mRNAs for endothelin-related proteins in human endometrium, myometrium and leiomyoma

Mol Cell Endocrinol. 1994 Jul;103(1-2):165-70. doi: 10.1016/0303-7207(94)90084-1.

Abstract

The expression of mRNAs encoding endothelin-1 (ET-1) and its receptors (ETA-R and ETB-R) as well as the ET degrading enzyme, neutral endopeptidase 24.11 (NEP), was determined in tissue samples of endometrium, myometrium and leiomyoma by using a reverse transcriptase polymerase chain reaction (RT-PCR) technique. ET-1 mRNA was detected in all samples studied. The level of ET-1 mRNA was higher in endometrium than in myometrium (p < 0.01) and leiomyoma (p < 0.001). The ETA-R mRNA was more abundant in endometrium than in myometrium (p < 0.001). For ETB-R mRNA there was no difference between these tissues. In contrast to ETA-R mRNA, which was more abundant in leiomyoma than in myometrium (p < 0.01), the ETB-R mRNA was less abundant in leiomyoma (p < 0.01). The NEP mRNA was detected in all endometrial samples but not in myometrium and leiomyoma. Our results show that the expression and relative levels of mRNAs encoding ET-1, ETA-R, ETB-R, and NEP vary in different tissue compartments of the human uterus. Since the net biological action of ET-1 in a particular cell type presumably depends on the balance between the peptide itself, its receptors and degrading enzymes, these results suggest different roles for ET-1 action in uterine endometrium, myometrium and leiomyoma. The difference in relative abundance of ETA-R and ETB-R mRNAs between myometrium and leiomyoma suggests that an altered ET-R gene expression may be a contributing factor in myomal growth.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • DNA, Complementary / chemistry
  • Endometrium / metabolism*
  • Endothelins / genetics*
  • Female
  • Gene Expression*
  • Humans
  • Leiomyoma / metabolism*
  • Molecular Sequence Data
  • Myometrium / metabolism*
  • Polymerase Chain Reaction
  • RNA, Messenger / metabolism*
  • Receptors, Endothelin / genetics*
  • Uterine Neoplasms / metabolism*

Substances

  • DNA, Complementary
  • Endothelins
  • RNA, Messenger
  • Receptors, Endothelin