MiR-155-5p plays as a“janus”in the expression of inflammatory cytokinesinduced by T-2 toxin
Food and Chemical Toxicology • 2020
Publication Information
Authors
Pu Guoa,c,1, Fang Qiaoa, 1, Deyu Huangb, Qinghua Wud,e, Tianlun Chenc, Sara Badawyc,Guyue Chengc, Haihong Haoc, Shuyu Xiec, Xu Wang
Keywords
T-2 toxin
microRNA-155
Inflammatory cytokines
Dual role
Journal
Food and Chemical Toxicology
Publisher
Elsevier
Volume
140
Issue
Not Available
Pages
111258
publication.type
International
Paper Link
Not Available
Supplementary Materials
Not Available
Abstract
Although many studies have shown that inflammatory response plays a crucial role in the various toxic effects of
T-2 toxin, there are relatively few reports on the mechanism of this phenomenon. Meanwhile, accumulating
evidence has shown that miR-155-5p is activated in the inflammatory response. As molecular pathways and
mechanisms involved in T-2 toxin-induced inflammatory response are poorly elucidated, we assessed whether
miR-155-5p is involved in the inflammation effects mediated by T-2 toxin. Treatment of RAW264.7 cells with T-
2 toxin (14 nM and 12 h) resulted in inflammatory response and associated with alteration of the gene expression
signature of miR-155-5p. Knockdown or overexpression of miR-155-5p both indicated that miR-155-5p positively regulated the expression of the inflammation factors. Moreover, bioinformatics prediction and luciferase
assay indicated that atg3 and rheb are targets of miR-155-5p. However, atg3 and SOCS1 play positive roles in the
inflammatory response regulated by miR-155-5p, while rheb plays a negative role. In addition, the in vivo study
showed that single administration of T-2 toxin in mice enhances spleen immune response, which was accompanied by an overexpression of miR-155-5p. These findings indicate that miR-155-5p might have an important
role associated with the inflammatory response induced by T-2 toxin. In conclusion, a dual character of miR-155-
5p in inflammation response was revealed, which might exist in other reactions in which miR-155-5p is involved.
T-2 toxin, there are relatively few reports on the mechanism of this phenomenon. Meanwhile, accumulating
evidence has shown that miR-155-5p is activated in the inflammatory response. As molecular pathways and
mechanisms involved in T-2 toxin-induced inflammatory response are poorly elucidated, we assessed whether
miR-155-5p is involved in the inflammation effects mediated by T-2 toxin. Treatment of RAW264.7 cells with T-
2 toxin (14 nM and 12 h) resulted in inflammatory response and associated with alteration of the gene expression
signature of miR-155-5p. Knockdown or overexpression of miR-155-5p both indicated that miR-155-5p positively regulated the expression of the inflammation factors. Moreover, bioinformatics prediction and luciferase
assay indicated that atg3 and rheb are targets of miR-155-5p. However, atg3 and SOCS1 play positive roles in the
inflammatory response regulated by miR-155-5p, while rheb plays a negative role. In addition, the in vivo study
showed that single administration of T-2 toxin in mice enhances spleen immune response, which was accompanied by an overexpression of miR-155-5p. These findings indicate that miR-155-5p might have an important
role associated with the inflammatory response induced by T-2 toxin. In conclusion, a dual character of miR-155-
5p in inflammation response was revealed, which might exist in other reactions in which miR-155-5p is involved.
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