Abstract
BackgroundAccumulated evidence reveals that cyclooxygenase-2 (COX-2) was overexpressed in eutopic endometrium of endometriosis, which may play a critical role in the pathogenesis of endometriosis. However, few studies have been performed to explore the molecular mechanisms underlying the abnormal high expression of COX-2 in endometriosis. Considering the fact that a number of recent studies have shown DNA methylation affecting some genes in endometriosis, the present study was therefore aimed to determine whether the observed high expression COX-2 in endometriosis is caused by the hypomethylation of CpG island within the promoter of this gene.MethodsThe endometrial tissues were collected from 60 women with endometriosis (endometriosis group) and 20 women without endometriosis (control group). The methylation status of COX-2 was examined by methylation specific PCR. Quantitative real-time RT-PCR was performed to measure COX-2 mRNA level in endometrial tissues.ResultsThe frequency of promoter hypermethylation of COX-2 was lower in eutopic endometrium of the endometriosis group (41.7%) than that in the control group (75.0%), P < 0.05. COX-2 mRNA level in the eutopic endometrium of the endometriosis group was 2.61-fold higher than that in the control group (P < 0.01). COX-2 mRNA level in unmethylated endometrium of the endometriosis group or the control group was 2.39-fold and 2.66-fold, respectively, higher than that in the methylated endometrium of the same group (P < 0.01).ConclusionsThe hypomethylation within the promoter of COX-2 may be responsible for the elevated gene expression in eutopic endometrium of endometriosis.
Highlights
Accumulated evidence reveals that cyclooxygenase-2 (COX-2) was overexpressed in eutopic endometrium of endometriosis, which may play a critical role in the pathogenesis of endometriosis
COX-2 mRNA expression in endometrial tissues To determine the correlation between DNA methylation and COX-2 expression in endometrial tissues, we evaluated the mRNA level of COX-2 in endometrial tissues between the endometriosis group and the control group by using quantitative real-time RT-PCR
Our data showed that the hypomethylation of nuclear factor responsible for the interleukin-6 expression (NF-IL6) site within COX-2 promoter may be responsible for the elevated gene expression in eutopic endometrium of endometriosis
Summary
Accumulated evidence reveals that cyclooxygenase-2 (COX-2) was overexpressed in eutopic endometrium of endometriosis, which may play a critical role in the pathogenesis of endometriosis. Few studies have been performed to explore the molecular mechanisms underlying the abnormal high expression of COX-2 in endometriosis. Endometriosis is an estrogen-dependent gynecological disorder that affects 6-10% of women of reproductive age. It is characterized histologically by the presence of endometrial tissue at sites outside of the uterine cavity, primarily on the pelvic peritoneum and ovaries, resulting in severe pelvic pain, pain during intercourse, and infertility [1,2]. We identified 10 up-regulated genes in the eutopic endometrium of endometriosis during the secretory phase using cDNA-RDA and found that cyclooxygenase-2 (COX-2) was one of the up-regulated genes [7]. The underlying mechanism of overexpression of COX-2 in eutopic endometrium of endometriosis has not been well defined
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