Participation of selected soluble cell adhesion molecules and syndecans in formation and development of endometriosis

Aleksandra Janusz1, Joanna Janusz1, Aleksandra Mielczarek-Palacz2

  • 1Department of Immunology and Serology, Faculty of Pharmaceutical Sciences in Sosnowiec, Medical University of Silesia, Katowice, Poland.

Ginekologia Polska
|July 15, 2021
PubMed
Abstract

Insights

Concentrations of soluble intercellular adhesion molecule (sICAM) and syndecan proteins in peritoneal fluid differ in women with endometriosis. These molecules may play a role in endometriosis development.

Area of Science:

  • Reproductive biology and immunology
  • Gynecology and obstetrics

Background:

  • Endometriosis is a complex gynecological condition.
  • Peritoneal fluid biomarkers for endometriosis are actively sought.
  • Soluble intercellular adhesion molecules (sICAMs) and syndecans are implicated in inflammatory and cellular processes.

Purpose of the Study:

  • To investigate the concentrations of soluble ICAM-2, -3, -4, and syndecan-1, -4 in the peritoneal fluid of women with endometriosis.
  • To determine if these molecules are associated with the formation and development of endometriosis.

Main Methods:

  • Study included 80 women (aged 21-49) undergoing laparoscopy.
  • 60 women diagnosed with endometriosis (pelvic) and 20 controls (no endometriosis).
  • Peritoneal fluid concentrations of sICAMs and syndecans were measured using ELISA.

Main Results:

  • Significantly decreased sICAM-2 and increased sICAM-3, sICAM-4, syndecan-1, and syndecan-4 concentrations were found in women with endometriosis compared to controls (p < 0.0001).
  • A negative correlation was observed between sICAM-3 and sICAM-2 concentrations in women with endometriosis.
  • No significant correlations were found between other tested sICAM and syndecan pairs.

Conclusions:

  • Altered concentrations of sICAMs and syndecans in peritoneal fluid are associated with endometriosis.
  • These molecules may influence immune response regulation, angiogenesis, and apoptosis of endometrial cells, contributing to endometriosis pathogenesis.

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