GENE EXPRESSION LEVELS OF GELATINASES IN ENDOMETRIOSIS

Mousazadeh, S and Khaksar, F (2018) GENE EXPRESSION LEVELS OF GELATINASES IN ENDOMETRIOSIS. The Journal of Urmia University of Medical Sciences, 28 (12). pp. 795-804.

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Abstract

Endometriosis is defined as the presence of tissue resembling endometrium outside the uterine cavity. Extensive remodeling existence in peritoneal mesothelium layer is necessary for adhesion, invasion, and proliferation of endometrial fragments, which is required the activation of matrix metalloproteinase (MMPs), as a normal menstrual cycle. MMPs are a family of zinc dependent endopeptidase that play important roles in the degradation of the extracellular matrix (ECM). It has been suggested that overexpression of MMP-2 and MMP-9 in endometriotic tissues may result in degradation of peritoneal ECM and providing the adhesion and invasion to develop endometriosis disease. Materials & Methods: For this purpose, we studied MMP-2,-9 expressions in ectopic and eutopic tissue samples of women undergoing laparoscopy for endometriosis and eutopic tissues of fertile women at Royan Institute. Twenty samples were used in each group and cDNAs were prepared from RNA which had been isolated from each sample. Real-time PCR was performed to measure the mRNA expression levels of MMP-2 and MMP-9. Results: Our results showed the overexpression of MMP-2 in ectopic and eutopic tissues of patients compared to the control group. However, statistical analysis showed no significant differences in the expression levels of MMP-2 between groups (P>0.05). The expression of MMP-9 in ectopic endometrium was significantly higher than that in eutopic and control group (P=0.012, P=0.014). Also, MMP-9 had high level of gene expression in eutopic samples compared with control group, but it did not reach the level (P>0.05). Conclusion: Overexpression of MMP-2 and MMP-9 in ectopic tissues of endometriosis may increase the strength of adhesion, invasion, and angiogenesis in the target tissue and improve endometriosis disease

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