Islet-cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfß signaling in mice.
FEBS Lett
; 594(17): 2881-2893, 2020 09.
Article
em En
| MEDLINE
| ID: mdl-32531799
ABSTRACT
Regeneration is a unique defense mechanism of liver tissue in response to functional cell loss induced by toxic chemicals or surgical resection. In this study, we found that Islet-cell autoantigen 69 (Ica69) accelerates liver regeneration in mice. Following 70% partial hepatectomy, both Ica69 mRNA and protein are significantly upregulated in mouse hepatocytes at the early stage of liver regeneration. Compared with the wild-type mice, Ica69-deficient mice have more severe liver injury, delayed liver regeneration, and high surgical accidental mortality following hepatectomy. Mechanistically, Ica69 interacts with Pick1 protein to regulate Tgfbr1 protein expression and Tgfß-induced Smad2 phosphorylation. Our findings suggest that Ica69 in liver tissue is a new potential target for promoting liver regeneration.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Autoantígenos
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Fator de Crescimento Transformador beta
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Hepatócitos
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Receptor do Fator de Crescimento Transformador beta Tipo I
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Fígado
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Regeneração Hepática
Limite:
Animals
Idioma:
En
Revista:
FEBS Lett
Ano de publicação:
2020
Tipo de documento:
Article
País de afiliação:
China