BPOZ-2-deficient mice exhibit aggravated inflammation-associated tissue damage after acute dextran sodium sulfate or diethylnitrosamine exposure.
Toxicol Lett
; 398: 49-54, 2024 Jul.
Article
em En
| MEDLINE
| ID: mdl-38866194
ABSTRACT
An excessive inflammatory response plays an important role in pathological tissue damage associated with pathogen infection and tumorigenesis. Blood POZ-containing gene type 2 (BPOZ-2), an adaptor protein for the E3 ubiquitin ligase scaffold protein CUL3, is a negative regulator of the inflammatory response. In this study, we investigated the pathophysiological functions of BPOZ-2 in dextran sodium sulfate (DSS)-induced colon injury and diethylnitrosamine (DEN)-induced liver damage. Our results indicated that BPOZ-2 deficiency increased IL-1ß induction after DSS and DEN treatment. In addition, BPOZ-2-deficient mice were more susceptible to DSS-induced colitis. Notably, BPOZ-2 deficiency aggravated DEN-induced acute liver injury. These results revealed that BPOZ-2 protected against pathological tissue damage with a dysregulated inflammatory response.
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Texto completo:
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Sulfato de Dextrana
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Colite
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Camundongos Knockout
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Dietilnitrosamina
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Doença Hepática Induzida por Substâncias e Drogas
Limite:
Animals
Idioma:
En
Revista:
Toxicol Lett
Ano de publicação:
2024
Tipo de documento:
Article