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International Journal of Fertility and Sterility، جلد ۹، شماره ۲.۵، صفحات ۲۱-۲۱

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عنوان انگلیسی I-43: Expression Profile of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway as A Potentional Biomarker in Pathophysiology of Endometriosis
چکیده انگلیسی مقاله Background: MIF via its receptor, CD74, initiates a signaling cascade that leads to proliferation and survival of cells. Also, MIF binding to CD74 activates p38 signaling pathways that lead to positive effect on the expression of COX-2. The aim of this study was to evaluate the gene expression profile of MIF, CD74 and COX-2 in normal, ectopic and eutopic endometrium during menstrual cycle. The expression level of MIF protein in peripheral blood samples of patients was another variable factor checked in this study. Materials and methods: Quantitative real-time polymerase chain reaction (Q-PCR) was performed using cDNA and primers for MIF, CD74 and COX-2. Also, protein level of MIF in blood serum was measured by ELISA assay. Results: The mean relative expression of MIF, CD74 and COX-2 genes were significantly higher in ectopic endometrium in compare to eutopic and control endometrium. However, there were significantly variations in mRNA expression of these genes in normal, ectopic and eutopic endometrium during menstrual cycle. Also women with endometriosis had significantly higher circulating levels of MIF protein as compared to normal controls. Conclusion: Higher expression of MIF, CD74 and COX-2 genes in ectopic endometrium can be considered as a molecular bi`omarker for endometriosis development and pathophysiology. Variation in the expression of these genes in normal, ectopic and eutopic endometrium during menstrual cycle could play an essential role in reproduction, inflammation and endometrium reconstruction.
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نویسندگان مقاله | m shahhoseini


s مهدیان | s mahdian


r سلمان یزدی | r salman yazdi


f رمضانعلی | f ramazanali


m اشرفی | m ashrafi


p افشاریان | p afsharian


r افلاطونیان | r aflatoonian



نشانی اینترنتی http://ijfs.ir/journal/article/abstract/4302
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