MiR-195 promotes myocardial fibrosis in MI rats via targeting TGF-β1/Smad

The aim of this study was to investigate the effect of micro ribonucleic acid (miR)-195 on myocardial infarction (MI) in rats via regulating the transforming growth factor-β1 (TGF-β1)/Smad signaling pathway. A total of 36 Sprague-Dawley rats were randomly divided into a normal group (n=12), a model group (n=12) and an miR-195 antagomir group (n=12). In the normal group, the heart was exposed only, and normal saline was intraperitoneally injected after operation. In the model group, the acute MI model was established. In the miR-195 antagomir group, the acute MI model was also established, and miR- 195 antagomir was intraperitoneally injected. The samples were collected at 2 weeks after surgery. Then cardiac function was detected via echocardiography, and the morphology of heart tissues was observed via hematoxylin and eosin (H&E) staining. Moreover, the expression of Collagen I was determined using immunohistochemistry, the protein expressions of TGF-β1, Smad3 and Smad7 were detected using Western blotting, and the expression of miR-195 was detected via quantitative polymerase chain reaction (qPCR). It was found by echocardiography that, compared with those in the normal group, left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) significantly declined, while left ventricular end-diastolic diameter (LVDd) and left ventricular end-systolic diameter (LVDs) significantly rose in the other two groups (P<0.05). In comparison with the model group, the miR-195 antagomir group had significantly increased LVEF and LVFS, and significantly decreased LVDd and LVDs (P<0.05). The immunohistochemistry results showed that the mean optical density of tissues with positively expressed Collagen I was obviously higher in the other two groups than that in the normal group (P<0.05), while it was obviously lower in the miR-195 antagomir group than that in the model group (P<0.05). According to the results of Western blotting, the protein expressions of TGF-β1 and Smad3 were evidently increased, while the protein expression of Smad7 was evidently decreased in the other two groups compared with those in the normal group (P<0.05). The opposite results were found in the miR-195 antagomir group compared with those in the model group (P<0.05). The results of qPCR manifested that the expression of miR-195 was markedly higher in the other two groups than that in the normal group (P<0.05), while it was markedly lower in the miR-195 antagomir group than in the model group (P<0.05). Moreover, it was observed using H&E staining that the myocardial fibers in the normal group had normal arrangement and intact structure, without obvious morphological abnormalities. In the model group, the myocardial fibers were arranged disorderly, and there were massive proliferating fibrous tissues, with a high degree of fibrosis. In themiR-195 antagomir group, the myocardial fibers were damaged and arranged less disorderly, and proliferation and fibrosis could be seen in some fibrous tissues, but to a lesser extent than the model group. In conclusion, miR-195 promotes myocardial fibrosis in MI rats via up-regulating the TGF-β1/Smad signaling pathway.