Figure - available from: World Journal of Urology
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iNOS increases the expression of HGF which promotes the differentiation of SCs by activating the p38/MAPK signaling pathway. a Expression of iNOS, HGF, p-p38 and p38 proteins in the SCs treated with pLenti-C-mGFP-iNOS, pLenti-C-mGFP-iNOS + DMSO or pLenti-C-mGFP-iNOS + SMT measured by western blot analysis. b Expression of iNOS and HGF mRNAs in the SCs treated with pLenti-C-mGFP-iNOS, pLenti-C-mGFP-iNOS + DMSO or pLenti-C-mGFP-iNOS + SMT detected by RT-qPCR. c, d Expression of HGF protein and mRNA in SCs transfected with siHGF measured by western blot analysis and RT-qPCR, respectively. e The protein levels of HGF, p-p38 and p38 in SCs after different treatments detected by western blot analysis. f The proliferation rate of SCs after different treatments assessed by CCK-8 assay. Independent sample t test was used to analyze the significant differences, *p < 0.05 vs. SCs treated with pLenti-C-mGFP-iNOS + DMSO
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PurposeSatellite cells (SCs) are multipotent skeletal muscle precursor cells, which can lead to muscle regeneration, a crucial process for the treatment of stress urinary incontinence (SUI). The activation of SCs is likely to be caused by inducible nitric oxide synthase (iNOS). This study examines the underlying mechanism of iNOS in SC activation,...
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Citations
... Pax7 is a specific marker of adult SCs. The activation of MyoD helps expand resting myogenic SCs (28,29). We first confirmed by immunofluorescence assay and Western blot assay that the expression of Pax7 and MyoD in SUI primary SCs was decreased (13). ...
Since the potential roles of extracellular vesicles secreted by adipose-derived mesenchymal stem cells (ADSCs) are not well understood in collagen metabolism, the purpose of this research was to evaluate the effects of ADSCs-extracellular vesicles in stress urinary incontinence and the regulatory mechanism of delivered microRNA-93 (miR-93). ADSCs were isolated and cultured, and ADSCs-extracellular vesicles were extracted and identified. Stress urinary incontinence primary fibroblasts or satellite cells were treated with ADSCs-extracellular vesicles to detect the expression of Elastin, Collagen I, and Collagen III in fibroblasts and Pax7 and MyoD in satellite cells. After transfecting ADSCs with miR-93 mimics or inhibitors, extracellular vesicles were isolated and treated with stress urinary incontinence primary fibroblasts or satellite cells to observe cell function changes. The online prediction and luciferase activity assay confirmed the targeting relationship between miR-93 and coagulation factor III (F3). The rescue experiment verified the role of ADSCs-extracellular vesicles carrying miR-93 in stress urinary incontinence primary fibroblasts and satellite cells by targeting F3. ADSCs-extracellular vesicles treatment upregulated expression of Elastin, Collagen I, and Collagen III in stress urinary incontinence primary fibroblasts and expression of Pax7 and MyoD in stress urinary incontinence primary satellite cells. miR-93 expression was increased in stress urinary incontinence primary fibroblasts or satellite cells treated with ADSCs-extracellular vesicles. Extracellular vesicles secreted by ADSCs could deliver miR-93 to fibroblasts and then negatively regulate F3 expression; ADSCs-extracellular vesicles could reverse the effect of F3 on extracellular matrix remodeling in stress urinary incontinence fibroblasts. miR-93 expression was also increased in stress urinary incontinence primary satellite cells treated by ADSCs-extracellular vesicles. Extracellular vesicles secreted by ADSCs were delivered to satellite cells through miR-93, which directly targets F3 expression and upregulates Pax7 and MyoD expression in satellite cells. Our study indicates that miR-93 delivered by ADSCs-extracellular vesicles could regulate extracellular matrix remodeling of stress urinary incontinence fibroblasts and promote activation of stress urinary incontinence satellite cells through targeting F3.
