miR-340-5p inhibits pancreatic acinar cell inflammation and apoptosis via targeted inhibition of HMGB1

被引:7
|
作者
Gao, Yazhou [1 ]
Wang, Liming [2 ]
Niu, Zequn [2 ]
Feng, Hui [2 ]
Liu, Jie [2 ]
Sun, Jiangli [2 ]
Gao, Yanxia [2 ]
Pan, Longfei [2 ]
机构
[1] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Emergency Med, Xian 710061, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Emergency Med, 157 Xiwu Rd, Xian 710004, Shaanxi, Peoples R China
关键词
microRNA-340-5p; high mobility group box 1; pancreatic acinar cells; apoptosis; inflammation; MOBILITY GROUP BOX-1; RECEPTOR; INJURY; ACTIVATION; EXPRESSION; PATHWAY; SEPSIS; RAGE; PATHOPHYSIOLOGY; MICRORNA;
D O I
10.3892/etm.2021.11063
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 pancreatitis (AP) is a common gastrointestinal disease that affects 1 million individuals worldwide. Inflammation and apoptosis are considered to be important pathogenic mechanisms of AP, and high mobility group box 1 (HMGB1) has been shown to play a particularly important role in the etiology of this disease. MicroRNAs (miRs) are emerging as critical regulators of gene expression and, as such, they represent a promising area of therapeutic target identification and development for a variety of diseases, including AP. Using the online database query (microRNA.org), the current study identified a site in the 3' untranslated region of HMGB1 mRNA that was a viable target for miR-340-5p. The present study aimed to investigate the association between miR-340-5p and HMGB1 expression in pancreatic acinar cells following lipopolysaccharide (LPS) treatment by performing luciferase, western blotting and reverse transcription-quantitative PCR assays. The results suggest that miR-340-5p attenuates the induction of HMGB1 by LPS, thereby inhibiting inflammation and apoptosis via blunted activation of Toll-like receptor 4 and enhanced AKT signaling. Thus, the therapeutic application of miR-340-5p may be a useful strategy in AP via upregulation of HMGB1 and subsequent promotion of inflammation and apoptosis.
引用
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页数:9
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