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miR-145 promotes the pathological process of acute Kawasaki disease by downregulating the target gene ACVR1B |
LYU Dianyi WU Fuxia CHEN Fengyi |
Department of Pediatrics, Yichang First People′s Hospital, Hubei Province, Yichang 443000, China |
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Abstract Objective To investigate the effect of down-regulation of ACVR1B gene by miR-145 in promoting the pathological process of acute Kawasaki disease (KD). Methods A total of 108 children who were treated in Yichang First People′s Hospital from November 2015 to June 2018 were included in the retrospective analysis, according to the disease conditions, children were divided into acute KD group (n = 28), with a confirmed diagnosis of acute KD; KD recovery group (n = 24), who was admitted to the hospital during the same period and in the recovery stage after treatment; pyrexia control group (n = 30), who had pyrexia due to upper respiratory tract infection; and normal control group (n = 26), who underwent physical examination during the same period. Serum was taken from the patients to check the expression level of miR-145. Target gene database was searched, and chemical-activated luciferase gene expression, qRT-PCR, and Western blot were performed. Results The white blood cell count, C-reactive protein, and erythrocyte sedimentation rate of acute KD group were significantly higher than the normal control group (P < 0.05), the acute KD group had significantly higher expression of miR-145 in serum than the KD recovery group, the pyrexia control group, and the normal control group (P < 0.05). The expression level of ACVR1B mRNA in serum of the fever control group was significantly lower than that of the normal control group (P < 0.05). The expression level of ACVR1B mRNA in serum of the acute KD group was significantly lower than that of the normal control group, the fever control group and the KD rehabilitation group (P < 0.05). Conclusion miR-145 can bind the 3′-UTR of ACVR1B and inhibit the expression of ACVR1B, and the regulatory relationship between miR-145 and ACVR1B can promote the pathological development of acute KD.
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