The upregulation of miR-204-3p in LPS-induced acute lung injury aggravated pulmonary endothelial cells apoptosis via targeting sulfatase 2

被引:5
|
作者
Zhang, Liya [1 ]
Zhu, Zhengyu [2 ]
Zhang, Qian [3 ]
Mao, Zhengdao [3 ]
机构
[1] Nanjing Med Univ, Dept Emergency Med, Affiliated Changzhou Peoples Hosp 2, Changzhou 213164, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Pediat, Affiliated Changzhou Peoples Hosp 2, Changzhou 213164, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Dept Resp Med, Affiliated Changzhou Peoples Hosp 2, Changzhou 213164, Jiangsu, Peoples R China
关键词
acute lung injury; sulfatase; 2; miR-204-3p; CANCER; INFLAMMATION; MICRORNAS;
D O I
10.18388/abp.2020_5518
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Acute lung injury (ALI) results from the injury of alveolar epithelial cells and pulmonary capillary endothelial cells, with a high mortality rate ranging from 29% to 42%. Therefore, more efficient therapeutic strategies for ALI are necessary. Numerous studies revealed that miRNAs play a role in the regulation of ALI. Lipopolysaccharide (LPS) can induce an inflammatory response and has been widely applied in the establishment of the mouse ALI model. Here, we reported that miR-204-3p expression was upregulated by LPS treatment with increased cytokine secretion. LPS treatment promoted cell apoptosis, accompanied by abnormal cell structure and unobvious alveolar structure. These effects could be prevented by down-regulation of miR-204-3p, and promoted by miR-204-3p overexpression. Sulfatase 2 (SULF2) appeared to be the target of miR-204-3p predicted by TargetScan. Downregulation of miR-204-3p enhanced the protein level of SULF2, indicating that SULF2 was a target of miR-204-3p, which could negatively regulate the expression of SULF2. Thus, targeting miR-204-3p may be a potential therapeutic strategy for ALI.
引用
收藏
页码:217 / 222
页数:6
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