The aim of the present study was to investigate the expression and mechanism of microRNA (miR)-93 in collagen expression in stress urinary incontinence (SUI). Vaginal tissue, primary fibroblasts and SUI primary fibroblasts were obtained to detect the expression of miR-93, interstitial collagenase (MMP1), collagen I and calpain-2. Reverse transcription-quantitative polymerase chain reaction analysis was performed to detect the levels of miR-93 and MMP1. Western blotting was used to evaluate the

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... rotein levels of calpain-2, MMP1 and collagen I. MMP1 and hydroxyproline levels in the supernatant were measured by ELISA. The association between miR-93 and calpain-2 was investigated by luciferase reporter assays. The expression of miR-93 and collagen I was significantly downregulated in the SUI group, while the expression of calpain-2 and MMP1 was significantly upregulated. ELISA analysis demonstrated that the MMP1 level increased and the hydroxyproline level decreased in the SUI group. Additionally, calpain-2 was identified to be a target of miR-93, and miR-93 was able to negatively regulate the expression of calpain-2. Restoration of calpain-2 in miR-93-overexpresseing SUI primary fibroblasts reversed the alteration in hydroxyproline expression, indicating that calpain-2 was negatively associated with collagen expression. The results of the present study suggested that miR-93 regulated MMP1 and collagen I expression in fibroblasts via calpain-2. miR-93 mediated collagen expression in stress urinary incontinence via calpain-2.