European review for medical and pharmacological sciences · 2018
MiR-1908 improves cardiac fibrosis after myocardial infarction by targeting TGF-β1.
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Chen Y, Li T, Gao Q, Wang L-Y, Cui L-Q
Аннотация
OBJECTIVE: To investigate the role and mechanism of micro ribonucleic acid (miR)-1908 in myocardial fibrosis after myocardial infarction.
MATERIALS AND METHODS: In in-vivo experiments, the rat model of myocardial infarction was established, and miR-1908 was up-regulated by lentivirus with miR-1908 overexpression. Cardiac function of rats was detected by echocardiography. Transforming growth factor-β1 (TGF-β1) and Smad2/3 expressions in infarction border zone were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Masson staining was used to detect the fibrosis, thus studying the role of miR-1908 in the myocardial fibrosis model. In in-vitro experiments, myocardial fibroblasts were isolated and cultured. Oxygen glucose deprivation (OGD) model was established to mimicking the ischemic condition; the relationship between miR-1908 and TGF-β1 was verified using luciferase reporter vector, lentivirus and small-interfering RNA (siRNA) in TGF-β1.
RESULTS: In-vivo experiments showed that the miR-1908 expression was down-regulated at 4 weeks after myocardial infarction. The up-regulation of miR-1908 significantly improved the cardiac function, reduced the myocardial fibrosis, and inhibited the expressions of TGF-β1 and Smad2/3. In-vitro experiments revealed that TGF-β1 was a target gene of miR-1908 and miR-1908 could inhibit the Smad2/3 expression through TGF-β1.
CONCLUSIONS: MiR-1908 can improve the myocardial fibrosis through the target gene TGF-β1.
MATERIALS AND METHODS: In in-vivo experiments, the rat model of myocardial infarction was established, and miR-1908 was up-regulated by lentivirus with miR-1908 overexpression. Cardiac function of rats was detected by echocardiography. Transforming growth factor-β1 (TGF-β1) and Smad2/3 expressions in infarction border zone were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Masson staining was used to detect the fibrosis, thus studying the role of miR-1908 in the myocardial fibrosis model. In in-vitro experiments, myocardial fibroblasts were isolated and cultured. Oxygen glucose deprivation (OGD) model was established to mimicking the ischemic condition; the relationship between miR-1908 and TGF-β1 was verified using luciferase reporter vector, lentivirus and small-interfering RNA (siRNA) in TGF-β1.
RESULTS: In-vivo experiments showed that the miR-1908 expression was down-regulated at 4 weeks after myocardial infarction. The up-regulation of miR-1908 significantly improved the cardiac function, reduced the myocardial fibrosis, and inhibited the expressions of TGF-β1 and Smad2/3. In-vitro experiments revealed that TGF-β1 was a target gene of miR-1908 and miR-1908 could inhibit the Smad2/3 expression through TGF-β1.
CONCLUSIONS: MiR-1908 can improve the myocardial fibrosis through the target gene TGF-β1.