Galectin-1 is over-expressed in endometriotic lesions from patients with minimal to mild endometriosis and promotes eutopic endometrial stromal cell proliferation.

BASTON JI; FERELLA L; CROCI D; HIDALGO P; BILOTAS M; RICCI A; BARAÑAO RI; SINGLA JJ; GONZALEZ A; JOHNSON MC; RABINOVICH G; MERESMAN G

Lisboa

Congreso; 31st Annual Meeting European Society of Human Reproduction (ESHRE); 2015

European Society of Human Reproduction (ESHRE)

Summary answer: The protein expression of Galectin-1 was significantly higher in endometriotic lesions than eutopic endometrium, and this increase occurred in patients with minimal to mild degree of endometriosis. The endogenous knock-down of Galectin-1 expression diminished cellular proliferation in eutopic endometrial stromal cells from patients with endometriosis but not from control women. What is known already: The pathophysiologic mechanisms involved in the aetiology of endometriosis are not entirely known yet. Galectin-1 is an endogenous lectin with binding-affinity for multiple N-acetyllactosamine disaccharides comprised on N- and O-glycans involved in several events of tumor biology. The potential pathophysiologic role of this lectin in human endometriosis has not yet been completely elucidated; however, we recently reported that Galectin-1 substantially contributes to endometriotic-like lesions growth and vascularization in an experimental endometriosis mouse model.Study design, size, and duration: All subjects were infertile women undergoing diagnostic laparoscopy, they showed regular menstrual cycles and had not received any hormonal medical treatment for the last three months. Endometriotic (n=41) and endometrial biopsies (n=27) were taken from women with endometriosis, and control women with tubal factor infertility, unexplained infertility or leiomyomas (n=27).Participants/materials, setting, methods: Biopsies of endometriotic lesions and eutopic endometrium were mechanically homogenized and Galectin-1 protein expression was assessed by Western blot. Knock-down of endogenous Galectin-1 expression was performed by RNA interference assay in primary cultures of eutopic endometrial stromal cells, and the cellular proliferation was measured by MTS method. Main results and the role of chance: There were no differences in the levels of Galectin-1 expression between eutopic endometrium from patients with endometriosis and controls (p=0.1037), but there was a significant increase of Galectin-1 expression in endometriotic lesions compared to eutopic endometrium from patients with endometriosis (p=0.0320). This increase occurs in patients with minimal to mild degree of endometriosis (p=0.0368), since in patients with moderate to severe endometriosis the endometriotic expression of this lectin did not differ significantly from eutopic endometrium (p=0.5573). On the other hand, the transient reduction of Galectin-1 expression in eutopic endometrial stromal cells has no apparent effect on cellular proliferation in primary cultures from control patients (p=0.2335), but the transient decrease of Galectin-1 expression caused a significant reduction of cellular proliferation in cultures from endometriosis patients (p=0.0061).Limitations, reasons for caution: More studies should be addressed to fully understand the mechanistic behind the results obtained and to evaluate the role of Galectin-1 in other events involved in the endometriosis pathophysiology.Wider implications of the findings: It is known that at early stages of the endometriosis development the ectopic lesions are highly metabolically active. The increased expression of Galectin-1 in endometriotic lesions from patients with minimal to mild degree of the disease besides the reduced cellular proliferation observed in Galectin-1 knock-down eutopic endometrial stromal cells from patients with endometriosis support the potential involvement of Galectin-1 in the endometriosis pathophysiology, and validate this lectin as a possible target for future therapeutic strategies.Study Funding: ANPCyT, CONICET and Fundación Roemmers, Buenos Aires, Argentina.