例如:"lncRNA", "apoptosis", "WRKY"

Effects of miR-150-5p on cerebral infarction rats by regulating the Wnt signaling pathway via p53.

Eur Rev Med Pharmacol Sci. 2020 Apr;24(7):3882-3891. doi:10.26355/eurrev_202004_20854
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摘要


OBJECTIVE:The aim of this study was to screen differentially expressed micro ribonucleic acids (miRNAs) in the plasma of patients with cerebral infarction (CI). In addition, the role of miR-150-5p in the incidence of CI is mainly explored via animal models and molecular biology experiments. PATIENTS AND METHODS:Blood samples were collected from hospitalized patients diagnosed with CI, including 15 CI patients and 15 non-CI patients as negative controls. Differentially expressed miRNAs in the plasma of these subjects were screened by microarray analysis. TargetScan was applied to predict the target genes of miR-150-5p, which were subjected to GO and pathway enrichment analyses using WebGestalt. Sprague-Dawley rats were randomly divided into Sham group (n=20), Control group (n=20), and Experimental group (n=20). CI model in rats was established in the latter two groups. Rats in Experimental group and Control group were intravenously injected with miR-150-5p mimics or miR-negative control (NC), respectively. The expressions of vital genes in the Wnt signaling pathway, including p53, Cyclin D1 (CCND1), c-Myc, β-catenin (CTNNB1) and Survivin were detected by Western blot in rats at 3 d after injection. RESULTS:A total of 3,568 differentially expressed miRNAs were detected in the peripheral blood between CI patients and controls, whose 2,100 were upregulated, including miR-150-5p (p<0.05). The target genes of miR-150-5p were involved in molecular pathways, such as the Wnt signaling pathway, carcinogenesis, endocrine regulation, and infection. Compared with rats in Control group, the protein expression of p53 was downregulated (p<0.05), while CCND1, c-Myc, CTNNB1 and Survivin were upregulated (p<0.05) in Experimental group. CONCLUSIONS:MiR-150-5p regulates the Wnt signaling pathway and participates in cell proliferation and apoptosis by downregulating p53, which may be a potential mechanism of CI induction.

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