Endometriosis is characterized by an impaired localization of laminin-5 and α3β1 integrin receptor

Gianluigi Giannelli, G Giannelli, Concetta Sgarra, C Sgarra, Sgarra C, E Di Naro, Edoardo Di Naro, Lavopa C, C Lavopa, Angelotti U, U Angelotti, Umberto Filippo Angelotti, M Tartagni, Massimo Tartagni, Simone O, O Simone, Olivia Simone, P Trerotoli, Paolo Trerotoli, Salvatore Antonaci, S Antonaci, Antonaci S, G Loverro, Giuseppe Loverro
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2006 · vol. 17(1) , pp. 242–247 · doi:10.1111/j.1525-1438.2006.00750.x · PMID:17291260 · W2001503719
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This study investigated the distribution of laminin-5 and its receptor, α3β1 integrin, in endometriosis tissue, finding their localization to be impaired.

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Abstract

Endometriosis is an estrogen-correlated benign disease characterized by a marked ability of endometrial-like cells to invade and proliferate outside uterine cavity, resembling for some invasive aspect the cancer growth. The molecular mechanisms regulating endometrial cell invasiveness are mostly unknown, although interactions between extracellular matrix (ECM) proteins and their transmembrane receptors, integrins, are likely to play a central role. In particular, laminin (Ln)-5 could be closely involved, as it is in cancer. We have investigated the expression of Ln-1, Ln-5, and collagen IV (Coll IV) ECM proteins and their receptors, alpha3beta1 and alpha6beta4 integrins, in atrophic, proliferative, and secretive endometrium and in endometriosis. The results show that Ln-5, but not Ln-I and Coll IV, is altered in secretive endometrium as well as in endometriosis tissues. No alterations are observed in atrophic or proliferative endometrium. Consistently, the polarization of both integrin subunits alpha3 and beta1, but not alpha6 and beta4, is altered in secretive endometrium and endometriosis tissues, but not in atrophic and proliferative endometrium. These results seem to suggest that Ln-5 and alpha3beta1 could be involved in the invasive mechanism of endometriosis. The altered expression of Ln-5, by upregulating matrix metalloproteases activity, suggest an invading process similar to that of many cancer processes.

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Condition tags

endometriosis

MeSH descriptors

Cell Adhesion Molecules Endometriosis Integrin alpha3beta1 Adult Basement Membrane Basement Membrane Cell Adhesion Molecules Cell Growth Processes Cell Growth Processes Collagen Type IV Collagen Type IV Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Humans Integrin alpha3beta1 Integrin alpha6beta4

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