MicroRNA20b5p promotes ventricular remodeling by targeting the TGFβ/Smad signaling pathway in a rat model of ischemiareperfusion injury
Myocardial ischemic injury results from severe impairment of the coronary blood supply and may lead to metabolic and ultrastructural changes, thereby causing irreversible damage. MicroRNA (miR)20b5p has been demonstrated to be involved in malignancies of the breast, colorectum, stomach, blood and oropharynx. The present study aimed to investigate the effects of miR20b5p on ventricular remodeling following myocardial ischemiareperfusion (IR) injury in rats by targeting small mothers against decapentaplegic homolog 7 (Smad7) via the transforming growth factorβ (TGFβ)/Smad signaling pathway. A total of 70 adult male SpragueDawley rats were divided into seven groups: Sham group, IR group, negative control group, miR20b5p mimics group, miR20b5p inhibitors group, small interfering RNA (siRNA)Smad7 group, and miR20b5p inhibitors + siRNASmad7 group. Dual luciferase reporter gene assays were used to verify the association between miR20b5p and Smad7. Myocardial infarction size, myocardial collagen volume fraction and perivascular collagen area were detected separately using triphenyltetrazolium chloride and Masson's staining. The rate of positive expression of Smad7 was detected using immunohistochemistry, and the expression levels of miR20b5p, TGFβ1, Smad3 and Smad7 were detected using reverse transcriptionquantitative polymerase chain reaction and western blot analyses. The findings revealed that miR20b5p inhibited Smad7. Compared with the sham group, the other six groups had increased myocardial infarction size, myocardial collagen, and expression of miR20b5p, TGFβ1 and Smad3, and decreased expression of Smad7. Compared with the IR group, the miR20b5p mimics group and the siRNASmad7 group had increased myocardial infarction size and myocardial collagen, increased expression of TGFβ1 and Smad3, and decreased expression of Smad7. The expression of miR20b5p was markedly increased in the miR20b5p mimics group, but did not differ significantly from that in the siRNASmad7 group. The results demonstrated that miR20b5p promoted ventricular remodeling following myocardial IR injury in rats by inhibiting the expression of Smad7 through activating the TGFβ/Smad signaling pathway.
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Document Type: Research Article
Affiliations: Department of Cardiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China
Publication date: January 1, 2018
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- The International Journal of Molecular Medicine is a monthly, peer-reviewed journal devoted to the publication of high quality studies related to the molecular mechanisms of human disease. The journal welcomes research on all aspects of molecular and clinical research, ranging from biochemistry to immunology, pathology, genetics, human genomics, microbiology, molecular pathogenesis, molecular cardiology, molecular surgery and molecular psychology.
The International Journal of Molecular Medicine aims to provide an insight for researchers within the community in regard to developing molecular tools and identifying molecular targets for the diagnosis and treatment of a diverse number of human diseases.
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