miR-22a targets p62/SQSTM1 to negatively affect autophagy and disease resistance of grass carp (Ctenopharyngodon idella)

被引:1
作者
Yu, Hongyan [1 ,2 ]
Xie, Lingli [1 ,2 ]
Chen, Zheyan [1 ,2 ]
Niu, Huiqin [1 ,2 ]
Jia, Xuewen [1 ,2 ]
Du, Biao [1 ,2 ]
Shen, Yubang [1 ,2 ,3 ]
Gui, Lang [1 ,2 ,3 ]
Xu, Xiaoyan [1 ,2 ,3 ]
Li, Jiale [1 ,2 ,3 ]
机构
[1] Shanghai Ocean Univ, Minist Agr & Rural Affairs, Key Lab Freshwater Aquat Genet Resources, Shanghai, Peoples R China
[2] Shanghai Ocean Univ, Shanghai Engn Res Ctr Aquaculture, Shanghai, Peoples R China
[3] Shanghai Ocean Univ, Natl Demonstrat Ctr Expt Fisheries Sci Educ, Shanghai, Peoples R China
关键词
Autophagy; miR-22a; Grass carp; Immune; P62; APOPTOSIS; MECHANISM; DOMAIN;
D O I
10.1016/j.fsi.2023.109124
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
MicroRNAs (miRNAs) are integral to many biological functions, including autophagy, a process recently proven to be closely linked to innate immunity. In this study, we present findings on miR-22a, a teleost homolog of mammalian miR-22, illustrating its capacity to target the autophagy adaptor p62, subsequently inducing downregulation at both mRNA and protein levels. Utilizing Western blot analyses, we demonstrated that miR22a inhibits the autophagy flux of CIK cells, correlated with an elevated presence of LC3 II. Additionally, the overexpression of miR-22a resulted in the suppression of NF-kappa B signaling, leading to reduced cellar antimicrobial abilities and increased apoptosis. These findings provide novel insights into the role of miR-22a as an autophagyrelated miRNA and its immune mechanisms against pathogens via p62 in teleost, enriching our understanding of the interplay between autophagy and innate immunity.
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页数:8
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