Long-term copper exposure caused hepatocytes autophagy in broiler via miR-455-3p-OXSR1 axis.
Chem Biol Interact
; 369: 110256, 2023 Jan 05.
Article
em En
| MEDLINE
| ID: mdl-36372260
ABSTRACT
Copper (Cu) is a common environmental pollutant which has been identified to cause toxic effects on animal bodies. MicroRNAs (miRNAs) are a type of non-coding RNAs involved in the regulation of various cellular activities including autophagy, but the potential regulatory mechanisms after excess Cu intake are still uncertain. Our previous study has prompted that Cu exposure reduced liver miR-455-3p levels. Herein, miR-455-3p was found to be an important molecule in the regulation of Cu-induced autophagy in vivo and in vitro. Histopathology observation of liver tissue indicated that Cu-induced severe hepatic damage including cellular swelling and vacuolization. Meanwhile, excessive Cu exposure not only heighten the mRNA and protein expression levels of Beclin1, Atg5, LC3â
and LC3â
¡, but also decreased miR-455-3p levels. In vitro experiment, Cu-induced autophagy can be attenuated by miR-455-3p overexpression. Additionally, oxidative stress-responsive 1 (OXSR1) was identified as a direct downstream target of miR-455-3p by dual luciferase reporter assays. Moreover, knockdown of OXSR1 can attenuate the autophagy induced by Cu treatment and the miR-455-3p inhibitor. Overall, the miR-455-3p-OXSR1 axis works as a regulator of autophagy under Cu stress, which provides a basis for further revealing the mechanism of chronic Cu poisoning.
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Texto completo:
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Cobre
/
MicroRNAs
Limite:
Animals
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article