Vol 92, No 11 (2021)
Research paper
Published online: 2021-06-24

open access

Page views 6468
Article views/downloads 664
Get Citation

Connect on Social Media

Connect on Social Media

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

Aleksandra Janusz1, Joanna Janusz1, Aleksandra Mielczarek-Palacz1, Justyna Sikora1, Aleksandra Englisz1, Marta Smycz-Kubanska1, Zdzislawa Kondera-Anasz1
Pubmed: 34263915
Ginekol Pol 2021;92(11):745-752.

Abstract

Objectives: Concentrations of soluble ICAM-2, -3, -4 and syndecan-1 and -4 have not yet been marked in the peritoneal fluid of women with endometriosis. The aim of the study was to determine whether these molecules can participate in formation and development of endometriosis.
Material and methods: The study comprised of 80 women at the proliferative phase of the menstrual cycle, aged 21 to 49 years (mean age 31. 3 ± 6. 7 years) undergoing laparoscopy, to determine the causes of primary infertility and to confirm or exclude endometriosis. The study group consisted of 60 women with endometriosis in the pelvis as confirmed by laparoscopy and histopathology. The reference group consisted of 20 women in whom no endometriosis. Concentrations of selected sICAM and syndecans in the peritoneal fluid were determined with the use of ELISA method.
Results: Decreased concentrations of sICAM-2 and increased concentrations of sICAM-3, sICAM-4 and syndnecan-1 and -4 were observed in the peritoneal fluid of women with endometriosis and compared with concentrations of this parameter in the reference group (p < 0.0001). Additionally, negative correlation was found between the concentrations of sICAM-3 and sICAM-2 among women with endometriosis. There was no statistically significant correlation between the concentration of sICAM-2 and sICAM-4, sICAM-3 and sICAM-4 and syndecan-1 and syndecan-4 in the examined women.
Conclusions: Changes in concentrations of all the evaluated molecules were observed in the peritoneal fluid in women suffering from endometriosis. Since they have a role in regulation of the immune response, in angiogenesis and apoptosis of the endometrial cells.

Article available in PDF format

View PDF Download PDF file

References

  1. Amsellem V, Dryden NH, Martinelli R, et al. ICAM-2 regulates vascular permeability and N-cadherin localization through ezrin-radixin-moesin (ERM) proteins and Rac-1 signalling. Cell Commun Signal. 2014; 12: 12.
  2. Bessa NZ, Francisco Dd, Andres Md, et al. Polymorphisms of ICAM-1 and IL-6 genes related to endometriosis in a sample of Brazilian women. J Assist Reprod Genet. 2016; 33(11): 1487–1492.
  3. Bohonyi N, Pohóczky K, Szalontai B, et al. Local upregulation of transient receptor potential ankyrin 1 and transient receptor potential vanilloid 1 ion channels in rectosigmoid deep infiltrating endometriosis. Mol Pain. 2017; 13: 1744806917705564.
  4. Carulli S, Beck K, Dayan G, et al. Cell surface proteoglycans syndecan-1 and -4 bind overlapping but distinct sites in laminin α3 LG45 protein domain. J Biol Chem. 2012; 287(15): 12204–12216.
  5. Chaireti R, Lindahl TL, Byström B, et al. Inflammatory and endothelial markers during the menstrual cycle. Scand J Clin Lab Invest. 2016; 76(3): 190–194.
  6. Chelariu-Raicu A, Wilke C, Brand M, et al. Syndecan-4 expression is upregulated in endometriosis and contributes to an invasive phenotype. Fertil Steril. 2016; 106(2): 378–385.
  7. Chung YM, Kim BG, Park CS, et al. Increased expression of ICAM-3 is associated with radiation resistance in cervical cancer. Int J Cancer. 2005; 117(2): 194–201.
  8. Cicinelli E, Trojano G, Mastromauro M, et al. Higher prevalence of chronic endometritis in women with endometriosis: a possible etiopathogenetic link. Fertil Steril. 2017; 108(2): 289–295.e1.
  9. Echtermeyer F, Streit M, Wilcox-Adelman S, et al. Delayed wound repair and impaired angiogenesis in mice lacking syndecan-4. J Clin Invest. 2001; 107(2): R9–RR14.
  10. Feduska JM, Aller SG, Garcia PL, et al. ICAM-2 confers a non-metastatic phenotype in neuroblastoma cells by interaction with α-actinin. Oncogene. 2015; 34(12): 1553–1562.
  11. Galvankar M, Singh N, Modi D. Estrogen is essential but not sufficient to induce endometriosis. J Biosci. 2017; 42(2): 251–263.
  12. Gorina R, Lyck R, Vestweber D, et al. β2 integrin-mediated crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular neutrophil diapedesis across the inflamed blood-brain barrier. J Immunol. 2014; 192(1): 324–337.
  13. Hyun YM, Hong CW. Deep insight into neutrophil trafficking in various organs. J Leukoc Biol. 2017; 102(3): 617–629.
  14. Izumi G, Koga K, Takamura M, et al. Involvement of immune cells in the pathogenesis of endometriosis. J Obstet Gynaecol Res. 2018; 44(2): 191–198.
  15. Johnson NP, Hummelshoj L, Adamson GD, et al. World Endometriosis Society Sao Paulo Consortium . World Endometriosis Society consensus on the classification of endometriosis. Hum Reprod. 2017; 32(2): 315–324.
  16. Kim YG, Kim MiJ, Lim JS, et al. ICAM-3-induced cancer cell proliferation through the PI3K/Akt pathway. Cancer Lett. 2006; 239(1): 103–110.
  17. Manthe RL, Muro S. ICAM-1-Targeted Nanocarriers Attenuate Endothelial Release of Soluble ICAM-1, an Inflammatory Regulator. Bioeng Transl Med. 2017; 2(1): 109–119.
  18. Pabalan N, Jarjanazi H, Christofolini DM, et al. Association of the intercellular adhesion molecule-1 (ICAM-1) gene polymorphisms with endometriosis: a systematic review and meta-analysis. Arch Gynecol Obstet. 2015; 292(4): 843–851.
  19. Palaiologou M, Delladetsima I, Tiniakos D. CD138 (syndecan-1) expression in health and disease. Histol Histopathol. 2014; 29(2): 177–189.
  20. Schneider C, Kässens N, Greve B, et al. Targeting of syndecan-1 by micro-ribonucleic acid miR-10b modulates invasiveness of endometriotic cells via dysregulation of the proteolytic milieu and interleukin-6 secretion. Fertil Steril. 2013; 99(3): 871–881.e1.
  21. Soilleux EJ. DC-SIGN (dendritic cell-specific ICAM-grabbing non-integrin) and DC-SIGN-related (DC-SIGNR): friend or foe? Clin Sci (Lond). 2003; 104(4): 437–446.
  22. Szatmári T, Ötvös R, Hjerpe A, et al. Syndecan-1 in Cancer: Implications for Cell Signaling, Differentiation, and Prognostication. Dis Markers. 2015; 2015: 796052.
  23. Park JK, Park SHo, So K, et al. ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB. Int J Oncol. 2010; 36(1): 181–192.