Journal Article
Research Support, Non-U.S. Gov't
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Differential expression profiling of matrix metalloproteinases and tissue inhibitors of metalloproteinases in females with or without pelvic organ prolapse.

Pelvic organ prolapse (POP) is a common disorder that can disturb the health and quality of life of females. However, the basic pathophysiology and underlying mechanism of POP are not fully understood. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) have been reported to be associated with the onset and development of POP. In the present study, to characterize the differential expression profile of MMPs and TIMPs in female patients with and without POP, a total of 72 POP patients were sampled as a patient group and 72 non-POP patients that underwent hysterectomy due to benign tumors were sampled as a control group. Immunohistochemistry and polymerase chain reaction analysis were used to detect the expression levels of MMP-1, -2, -3 and -9 as well as TIMP-1 protein and mRNA in the anterior vaginal wall tissues. The expression levels of MMP-1, -2, -3 and -9 in the patient group were found to be significantly higher than those in the control group. By contrast, TIMP-1 expression levels in the patient group were significantly lower than those in the control group. Correlational analysis revealed a significantly positive correlation among the expression levels of MMP-2, -3 and -9. TIMP-1 expression levels were significantly negatively correlated with the expression levels of MMP-3 and -9. In addition, the expression levels of MMP-1 exhibited a positive correlation with those of MMP-2, -3 and -9, but a negative correlation with those of TIMP-1. The results demonstrated that the increased expression levels of MMPs and the reduced expression levels of TIMPs were directly associated with the presence of uterine prolapse, indicating that the differential expression levels of MMPs and TIMPs were correlated with the occurrence and development of POP. This data may assist in elucidating the molecular mechanism of MMP and TIMP involvement in POP, and also provide an underlying theoretical basis for the prevention and treatment of POP.

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