miRNA-1246 suppresses acute lung injury-induced inflammation and apoptosis via the NF-κB and Wnt/β-catenin signal pathways

被引:59
作者
Suo, Tao [1 ]
Chen, Guo-zhong [1 ]
Huang, Yi [1 ]
Zhao, Kao-chang [1 ]
Wang, Tao [1 ]
Hu, Ke [1 ]
机构
[1] Wuhan Univ, Renmin Hosp, Div Resp Dis, Zhangzhidong Rd 99, Wuhan 430060, Hubei, Peoples R China
关键词
miRNA-1246; ALI; Inflammation; Apoptosis; NF-kappa B; Wnt/beta-catenin; RESPIRATORY-DISTRESS-SYNDROME; DOWN-REGULATION; CLINICAL-TRIAL; MICE; INHIBITION; MICRORNAS; CELLS; MACROPHAGES; ACTIVATION; BIOMARKERS;
D O I
10.1016/j.biopha.2018.09.046
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Acute lung injury (ALI) is the common and complicated inflammatory lung disease. MicroRNAs (miRNA) have emerged as novel gene regulatory molecules which play a crucial role in multiple complicated diseases, including ALI. In this study, we aims to identify potential regulatory functions of miRNA-1246 in lipopolysaccharide (LPS)-induced ALI. In ALI mice, miRNA-1246 expression is effectively up-regulated, compared with the control group. miRNA-1246 overexpression effectively increases inflammation and apoptosis of in vitro ALI model. In contrast, miRNA-1246 knockdown effectively inhibits inflammation and cell apoptosis in vitro ALI model. Furthermore, up-regulation of miRNA-1246 significantly induces nuclear factor-kappa B (NF-kappa B) protein expression, and suppresses Wnt and beta-catenin protein expression in vitro ALI model. Following the inhibition of NF-kappa B or Wnt/beta-catenin signal using inhibitors, miRNA-1246 shows no significant effects on ALI-induced inflammation and apoptosis. Taken together, miRNA-1246 mediates ALI-induced lung inflammation and apoptosis via the NF-kappa B activation and Wnt/beta-catenin suppression.
引用
收藏
页码:783 / 791
页数:9
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