miR-22a targets p62/SQSTM1 to negatively affect autophagy and disease resistance of grass carp (Ctenopharyngodon idella)
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, s...
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Published in | Fish & shellfish immunology Vol. 142; p. 109124 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Ltd
01.11.2023
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1050-4648 1095-9947 |
DOI: | 10.1016/j.fsi.2023.109124 |