Endometrial leptin and leptin receptor expression in women with severe/moderate endometriosis

Mol Hum Reprod. 2004 Nov;10(11):777-82. doi: 10.1093/molehr/gah115. Epub 2004 Oct 1.

Abstract

The leptin system has been implicated in reproductive function, acting at endocrine and paracrine levels. Recently, deregulation of this gene family has been linked to endometrial changes caused by endometriosis. In the present study, we compare the expression of leptin receptor mRNA during the pre-receptive (LH+2) and receptive (LH+9) phases in the eutopic endometrium from patients with severe/moderate endometriosis (n = 30) versus fertile controls (n = 12). In each patient, two endometrial samples were obtained at LH+2 and LH+9 in their natural cycles. When real-time quantitative fluorescent PCR was performed, an up-regulation of OB-RL and all the isoforms investigated was observed at LH+9 versus LH+2 in patients with and without endometriosis. However, no difference was found in the expression pattern of the total leptin receptor OB-RT, or in its long OB-RL and soluble HuB219.3 forms when the eutopic endometria of patients with severe/moderate endometriosis and fertile controls were compared. By means of in situ hybridization, total leptin receptor mRNA was localized in the luminal epithelium and the glands of the endometrium. The immunohistochemical analysis of the long form of leptin receptor was also performed in order to confirm these findings at the protein level. Finally, we have also shown similar leptin mRNA expression in both the control group and patients with endometriosis. In conclusion, we have not identified differences in the endometrial expression and localization of leptin and the leptin receptor when comparing the eutopic endometrium of women with severe/moderate endometriosis and fertile controls.

Publication types

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

MeSH terms

  • Adult
  • Endometriosis / genetics
  • Endometriosis / metabolism*
  • Endometrium / chemistry
  • Endometrium / metabolism*
  • Endometrium / pathology
  • Female
  • Gene Expression
  • Humans
  • In Situ Hybridization
  • Leptin / genetics
  • Leptin / metabolism*
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • RNA, Messenger / analysis
  • RNA, Messenger / metabolism
  • Receptors, Cell Surface / analysis
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism*
  • Receptors, Leptin
  • Reverse Transcriptase Polymerase Chain Reaction
  • Up-Regulation*

Substances

  • LEPR protein, human
  • Leptin
  • Protein Isoforms
  • RNA, Messenger
  • Receptors, Cell Surface
  • Receptors, Leptin