The lncRNA H19 Mediates Pulmonary Fibrosis by Regulating the miR-196a/COL1A1 Axis

被引:81
|
作者
Lu, Qingchun [1 ]
Guo, Zhongliang [1 ]
Xie, Wang [1 ]
Jin, Wenjing [2 ]
Zhu, Dongyi [1 ]
Chen, Song [3 ]
Ren, Tao [4 ]
机构
[1] Tongji Univ, Sch Med, Dept Resp Med, Shanghai East Hosp, Shanghai 200120, Peoples R China
[2] Fudan Univ, Pudong Med Ctr, Dept Intens Care Unit, Shanghai Pudong Hosp, Shanghai 201399, Peoples R China
[3] Shanghai Pudong New Area Peoples Hosp, Dept Emergency & Crit Care Med, Shanghai 201299, Peoples R China
[4] Shanghai Jiao Tong Univ, Dept Resp Med, Affiliated Peoples Hosp 6, Shanghai 200233, Peoples R China
基金
中国国家自然科学基金;
关键词
long noncoding RNA; H19; miR-196a; competing endogenous RNA; lung fibrosis; COL1A1; LONG NONCODING RNAS; CANCER-CELL; EXPRESSION; PROGRESSION; MECHANISMS; MICRORNAS;
D O I
10.1007/s10753-018-0744-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Idiopathic pulmonary fibrosis (IPF) is characterized by lung fibroblasts accumulation and extracellular matrix (ECM) deposition. Recently, long-noncoding RNAs (lncRNAs) have emerged as critical regulators and prognostic markers in several diseases including IPF. In the present study, we found that the expression of H19 was significantly increased in transforming growth factor-beta (TGF-beta)-induced fibroblast proliferation and bleomycin-(BLM) induced lung fibrosis (p < 0.05). We further demonstrated that H19 was a direct target of miR-196a and was associated with COL1A1 expression by sponging miR-196a. Moreover, downregulation of H19 alleviated fibroblast activation and lung fibrosis, and this effect was blocked by a miR-196a inhibitor. In conclusion, our results suggest that lncRNA H19 has a promotive effect on BLM-induced IPF, and it functions as a molecular sponge of miR-196a, which provides a novel therapeutic target for IPF.
引用
收藏
页码:896 / 903
页数:8
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