详细信息

MiR-212-3p inhibits LPS-induced inflammatory response through targeting HMGB1 in murine macrophages  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:MiR-212-3p inhibits LPS-induced inflammatory response through targeting HMGB1 in murine macrophages

作者:Chen, Weiwei[1,2];Ma, Xiaoying[1,2];Zhang, Peng[1,2];Li, Qifeng[3];Liang, Xin[1,2];Liu, Jianwen[1,2]

机构:[1]East China Univ Sci & Technol, Sch Pharm, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, Shanghai, Peoples R China;[3]Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Pediat Neurosurg, Shanghai 200092, Peoples R China

年份:2017

卷号:350

期号:2

起止页码:318

外文期刊名:EXPERIMENTAL CELL RESEARCH

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000392461700003)】;

基金:This work was supported by the National Natural Science Foundation of China (Number: 8150254081502600) and the Program of Shanghai Health and Family Planning Commision (Number: 201440495).

语种:英文

外文关键词:MiR-212-3p; HMGB1; Inflammatory response; MAPKs

摘要:Sepsis is a major cause of mortality in seriously ill patients characterized by a series of severe systemic inflammatory responses due to an infection. Thus, there is a critically need to search more accurate biomarkers and targets for diagnosis and treatment of sepsis. Our study showed that miR-212-3p was up-regulated in LPS-treated macrophage RAW264.7 cells. Overexpression of miR-212-3p in RAW264.7 cells led to suppression of pro-inflammatory cytokines (TNF-alpha and IL-6) induced by LPS. Bioinformatic predictions and experimental researches both revealed that HMGB1 was a direct target of miR-212-3p. Meanwhile, the results showed that overexpression of miR-212-3p inhibited the cytoplasmic translocation of HMGB1 in LPS-induced RAW264.7 cells. Subsequently, transfection of the pcDNA3.1/HMGB1 plasmid, which produced HMGB1 overexpression, exhibited similar effects as the LPS-induced macrophage inflammatory response and markedly activated the MAPKs including p38, ERK and JNK phosphorylation. Furthermore, we also found that the phosphorylation of p38 MAPK and ERK was downregulated by miR-212-3p mimics upon LPS injection. In conclusion, these results reveal that miR-212-3p directly targets HMGB1 to suppress inflammatory response in LPS-induced RAW264.7 cells. All our findings indicate that miR-212-3p may act as a potential pharmacological target for promising and effective therapeutic intervention in microbial infection in the future.

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