MicroRNA-221-5p Promotes Ricin Toxin-induced Inflammation via PI3K/Akt signaling pathway by targeting COL4a5

被引:4
作者
Zhao, Na [1 ]
Yu, Haotian [1 ]
Xi, Yanli [2 ]
Dong, Mingxin [1 ]
Wang, Yan [1 ]
Sun, Chengbiao [1 ]
Zhang, Jianxu [1 ]
Xu, Na [2 ]
Liu, Wensen [1 ]
机构
[1] Chinese Acad Agr Sci, Changchun Vet Res Inst, Changchun 130122, Peoples R China
[2] Jinlin Med Univ, Jilin 132013, Jilin, Peoples R China
关键词
Ricin toxin; miRNAs; Inflammation; PI3K/Akt; COL4a5; ACUTE LUNG INJURY; MESSENGER-RNA; A-CHAIN; ENDOPLASMIC-RETICULUM; EXTRACELLULAR-MATRIX; OXIDATIVE STRESS; EXPRESSION; APOPTOSIS; MECHANISM; NETWORK;
D O I
10.1016/j.toxicon.2022.03.010
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Ricin toxin (RT) is one of the most lethal type II ribosome-inactivating proteins (RIP), and is classified as a potential bioterror agent due to its severe cytotoxicity and high availability. The toxicity of RT is dependent on both dose and route of exposure. Increasing evidence demonstrates that sub-lethal RT induces acute inflammation and increases the release of pro-inflammatory cytokines. However, current studies on mechanism of RTinduced inflammation are limited. In this study, to evaluate the relationship between miRNAs and RT-induced inflammation, RNA sequencing (RNA-Seq) was used to analyze the expression of miRNAs and mRNAs in RTtreated RAW264.7 macrophage cells. A total of 14 significantly differently expressed (DE) miRNAs and 323 miRNA-mRNA interaction pairs were predicted by bioinformatics analysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that majority of those interaction pairs were involved in PI3K/Akt pathway. In addition, overexpression of miR-221-5p promoted the inflammatory response by inhibiting the mRNA expression of COL4a5. This work contributes to our understanding of RT-induced inflammation and demonstrates the potential role of miRNAs in innate immunity, which may be regarded as potential targets in developing therapies for RT poisoning.
引用
收藏
页码:11 / 18
页数:8
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