Literature DB >> 10655459

Adhesion of menstrual endometrium to extracellular matrix: the possible role of integrin alpha(6)beta(1) and laminin interaction.

C A Koks1, P G Groothuis, G A Dunselman, A F de Goeij, J L Evers.   

Abstract

Previous in-vitro studies have shown that the endometrium preferentially adheres to the extracellular matrix (ECM) of the amnion and peritoneum. This interaction probably involves adhesion molecules, e.g. integrins. We evaluated the expression of integrins in naturally shed menstrual endometrium and the adhesion pattern of this tissue to different components of the ECM. To identify integrins and matrix components involved, blocking studies were performed. Most of the 15 menstrual tissue samples showed positive staining for each of the integrins investigated, except alpha(4)beta(1). Compared with binding to collagen IV, which was set at 100%, adhesion to collagen I was 93% (not significant), to fibronectin 87% (P < 0.05), and to laminin 74% (P < 0.05). Scanning electron micoscopy showed that endometrium adhered to laminin but hardly spread, whereas spreading was observed when layered on the other coatings. Compared with the control (which was set at 100%), incubation with 4B4, a monoclonal antibody against the integrin beta(1) subunit, showed a significant reduction of adhesion (to approximately 50%; P < 0.05) when layered on laminin and a smaller reduction (to 82-86%; P < 0.05) when layered on the other three coatings. Incubation with antibody GOH3 against integrin alpha(6)beta(1) resulted in a similar reduction in adhesion to laminin. Incubation with an RGD peptide significantly reduced adhesion (to 84%; P < 0.05) when plated on fibronectin. In conclusion, antegradely shed menstrual endometrium expresses various integrins. It shows preferential attachment to collagen IV and collagen I, when compared with fibronectin and laminin. Blockage of the integrin beta(1) subunit resulted in greatest disruption to adhesion when layered on laminin, implying that the interaction was mediated by the alpha(6)beta(1) integrin. Since this adhesion was not completely blocked, other mechanisms are likely to be involved.

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Year:  2000        PMID: 10655459     DOI: 10.1093/molehr/6.2.170

Source DB:  PubMed          Journal:  Mol Hum Reprod        ISSN: 1360-9947            Impact factor:   4.025


  7 in total

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Journal:  Reprod Med Biol       Date:  2005-05-03

2.  Stromal cells from endometriotic lesions and endometrium from women with endometriosis have reduced decidualization capacity.

Authors:  Petra A B Klemmt; Janet G Carver; Stephen H Kennedy; Philippe R Koninckx; Helen J Mardon
Journal:  Fertil Steril       Date:  2006-03       Impact factor: 7.329

3.  Molecular profiling of experimental endometriosis identified gene expression patterns in common with human disease.

Authors:  Idhaliz Flores; Elizabeth Rivera; Lynnette A Ruiz; Olga I Santiago; Michael W Vernon; Caroline B Appleyard
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4.  Selective inhibition of prostaglandin E2 receptors EP2 and EP4 inhibits adhesion of human endometriotic epithelial and stromal cells through suppression of integrin-mediated mechanisms.

Authors:  JeHoon Lee; Sakhila K Banu; Robert C Burghardt; Anna Starzinski-Powitz; Joe A Arosh
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Review 5.  Is abnormal eutopic endometrium the cause of endometriosis? The role of eutopic endometrium in pathogenesis of endometriosis.

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Journal:  Med Sci Monit       Date:  2011-04

Review 6.  Molecular aspects of development and regulation of endometriosis.

Authors:  Yana B Aznaurova; Marat B Zhumataev; Tiffany K Roberts; Alexander M Aliper; Alex A Zhavoronkov
Journal:  Reprod Biol Endocrinol       Date:  2014-06-13       Impact factor: 5.211

7.  Transforming growth factor β1 enhances adhesion of endometrial cells to mesothelium by regulating integrin expression.

Authors:  Hee-Jung Choi; Mi-Ju Park; Bo-Sung Kim; Hee-Jin Choi; Bosun Joo; Kyu Sup Lee; Jung-Hye Choi; Tae-Wook Chung; Ki-Tae Ha
Journal:  BMB Rep       Date:  2017-08       Impact factor: 4.778

  7 in total

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