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

• Published in: Fish & shellfish immunology Vol. 142; p. 109124
• Main Authors: Yu, Hongyan, Xie, Lingli, Chen, Zheyan, Niu, Huiqin, Jia, Xuewen, Du, Biao, Shen, Yubang, Gui, Lang, Xu, Xiaoyan, Li, Jiale
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.11.2023
• Subjects: Autophagy; Grass carp; Immune; miR-22a; Grass carp; Autophagy; miR-22a; Immune
• ISSN: 1050-4648; 1095-9947
• DOI: 10.1016/j.fsi.2023.109124

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 miR-22a 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-κB signaling, leading to reduced cellar antimicrobial abilities and increased apoptosis. These findings provide novel insights into the role of miR-22a as an autophagy-related miRNA and its immune mechanisms against pathogens via p62 in teleost, enriching our understanding of the interplay between autophagy and innate immunity. •miR-22a could block grass carp autophagy flux by simultaneously targeting grass carp p62.•miR-22a could be downregulated, while p62 could be upregulated by A.hydrophila stimulation in grass carp spleen and kidney.•miR-22a could increase the cellular bacterial adhesion, negatively regulate NF-κB signaling and weaken cell viability.