Deficient expression of tumor necrosis factor receptor type 2 in the endometrium of women with endometriosis

Am J Reprod Immunol. 2003 Jul;50(1):33-40. doi: 10.1034/j.1600-0897.2003.00058.x.

Abstract

Problem: Tumor necrosis factor-alpha (TNF-alpha) is secreted mainly during the menstrual phase and has been suggested to play a role in induction of apoptosis in endometrial cells and menstrual shedding. TNF-alpha receptor type 2 (TNF-RII) is believed to play a central role in TNFalpha-mediated cytotoxic, mitogenic, anti-proliferative and apoptotic effects. The aim of this study was to assess whether TNF-RII maybe expressed differentially in the endometrium of women with different degrees of endometriosis.

Method of study: TNF-RII expression in the endometrial tissue of women with and without endometriosis was investigated by immunohistochemical techniques and in situ hybridization.

Results: In histological sections, we observed TNF-RII mRNA and the corresponding protein localized mainly in endometrial glandular cells, with only very faint immunostaining in the surrounding stromal cells. Statistical analysis of our data showed a significant decrease in protein and mRNA expression of TNF-RII in endometrial glandular cells of patients with stages I and II endometriosis compared to normal subjects. TNF-RII expression was also found to decrease significantly in the secretory phase of the menstrual cycle in women with early endometriosis stages (I and II).

Conclusions: In view of the relevant role of TNF-RII in the modulation of the inflammatory and the proapoptotic effects of TNFalpha, deficient expression of TNF-RII mRNA in the endometrium of women at the earliest stages of endometriosis may play a significant role in the pathophysiology of this disease.

Publication types

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

MeSH terms

  • Adult
  • Antigens, CD / genetics
  • Antigens, CD / metabolism*
  • Endometriosis / metabolism*
  • Endometriosis / pathology
  • Endometrium / chemistry
  • Endometrium / metabolism*
  • Endometrium / pathology
  • Female
  • Gene Expression
  • Humans
  • Immunohistochemistry / methods
  • In Situ Hybridization, Fluorescence / methods
  • RNA, Messenger / metabolism
  • Receptors, Tumor Necrosis Factor / genetics
  • Receptors, Tumor Necrosis Factor / metabolism*
  • Receptors, Tumor Necrosis Factor, Type II
  • U937 Cells

Substances

  • Antigens, CD
  • RNA, Messenger
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type II