OBJECTIVE: Cardiovascular disease is one of the diseases threatening human health. Myocardial fibrosis is a major cause of cardiovascular diseases. Studies have shown that over expression of miR-203 can inhibit the fibrosis. Therefore, in this study, the effect of differential expression of miR-203 on fibrosis of cultured mouse cardiomyocytes was investigated. MATERIALS AND METHODS: Activators and inhibitors of miR-203 were designed according to the sequence of miR-203, synthesized, and transfected into mouse cardiomyocytes to establish activator group, inhibitor group, and control group. The expression levels of fibrosis-related factors including FN, CTGF, and TGF-β1 were measured by Western blot and RT-PCR 24 h and 36 h after transfection. RESULTS: Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN in a time-dependent manner, compared with that in the control group (p <0.05). Inhibition of miR-203 expression in mouse cardiomyocytes significantly increased the expression levels of TGF-β1, CTGF, and FN 36 h after transfection, compared with that in the control group (p < 0.05). No significant differences were seen in the expression levels of TGF-β1, CTGF, and FN 24 h after transfection, compared with that in the control group (p >0.05). CONCLUSIONS: Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN, which might be used as a detection index for prediction of fibrosis.
OBJECTIVE:Cardiovascular disease is one of the diseases threatening human health. Myocardial fibrosis is a major cause of cardiovascular diseases. Studies have shown that over expression of miR-203 can inhibit the fibrosis. Therefore, in this study, the effect of differential expression of miR-203 on fibrosis of cultured mouse cardiomyocytes was investigated. MATERIALS AND METHODS: Activators and inhibitors of miR-203 were designed according to the sequence of miR-203, synthesized, and transfected into mouse cardiomyocytes to establish activator group, inhibitor group, and control group. The expression levels of fibrosis-related factors including FN, CTGF, and TGF-β1 were measured by Western blot and RT-PCR 24 h and 36 h after transfection. RESULTS: Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN in a time-dependent manner, compared with that in the control group (p <0.05). Inhibition of miR-203 expression in mouse cardiomyocytes significantly increased the expression levels of TGF-β1, CTGF, and FN 36 h after transfection, compared with that in the control group (p < 0.05). No significant differences were seen in the expression levels of TGF-β1, CTGF, and FN 24 h after transfection, compared with that in the control group (p >0.05). CONCLUSIONS: Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN, which might be used as a detection index for prediction of fibrosis.
Authors: Debora Cristina Pereira da Silva; Felipe Demani Carneiro; Kelly Costa de Almeida; Caroline Fernandes-Santos Journal: Arq Bras Cardiol Date: 2018-11 Impact factor: 2.000