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miR-23a regulates the disease resistance of grass carp (Ctenopharyngodon idella) by targeting autophagy-related genes, ATG3 and ATG12
miRNAs play a key role in the autophagy process. In recent years, the emerging role of autophagy in regulating immune response has attracted increasing attention. Since then, specific miRNAs have also been found to play an immune function indirectly by modulating autophagy as well. This study proved...
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Published in: | Fish & shellfish immunology 2023-07, Vol.138, p.108812-108812, Article 108812 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | miRNAs play a key role in the autophagy process. In recent years, the emerging role of autophagy in regulating immune response has attracted increasing attention. Since then, specific miRNAs have also been found to play an immune function indirectly by modulating autophagy as well. This study proved that miR-23a could downregulate grass carp autophagy simultaneously by targeting ATG3 and ATG12. Besides, both ATG3 and ATG12 mRNA levels were increased in kidney and intestine after being infected by Aeromonas hydrophila; yet almost at the same time, miR-23a was decreased. Besides, we illustrated that grass carp miR-23a could affect antimicrobial capacity, proliferation, migration, and antiapoptotic abilities of CIK cells. These results indicate that miR-23a was related to grass carp autophagy and plays an important role in antimicrobial immunity through targeting ATG3 and ATG12, which provides important information on autophagy-related miRNAs about the defense and immune mechanisms against pathogens in teleost.
•miR-23a could interfere with grass carp autophagy by simultaneously targeting gcATG3 and gcATG12.•miR-23a could be downregulated, while gcATG3 and gcATG12 could be upregulated by A. hydrophila stimulation.•miR-23a could increase the adhesion of A. hydrophila, and weaken the cellular survivability of CIK cells. |
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ISSN: | 1050-4648 1095-9947 |
DOI: | 10.1016/j.fsi.2023.108812 |