ENO1 regulates IL-1ß-induced chondrocyte inflammation, apoptosis and matrix degradation possibly through the potential binding to CRLF1.
Tissue Cell
; 90: 102504, 2024 Oct.
Article
em En
| MEDLINE
| ID: mdl-39116531
ABSTRACT
In this study, we aim to investigate the role of enolase 1 (ENO1) in osteoarthritis (OA) pathogenic process and to uncover the underlying mechanism. To this end, we used IL-1ß to induce an in vitro OAlike chondrocyte model in human immortalized chondrocyte C-28/I2 cells. We manipulated the expression of ENO1 and cytokine receptor-like factor 1 (CRLF1) in IL-1ß-induced C-28/I2 cells using siRNA and/or overexpression and tested their effects on IL-1ß-induced pathologies including cell viability, apoptosis and inflammatory cytokine levels (IL-6 and TNF-α), and the expression of extracellular matrix-related enzymes and major mediators in the NF-κB signaling pathway (p-p65, p65, p-IκBα and IκBα). We used co-immunoprecipitation and immunofluorescence imaging to study a possible binding between ENO1 and CRLF1. Our data showed that IL-1ß induction elevated ENO1 and CRLF1 expression in C-28/I2 cells. Silencing ENO1 or CRLF1 inhibited the IL-1ß-induced cell viability damage, apoptosis, inflammation, and extracellular matrix degradation. The inhibitory effect of silencing ENO1 was reversed by CRLF1 overexpression, suggesting a functional connection between ENO1 and CRLF1, which could be attributed to a binding between these two partners. Our study could help validate the role of ENO1 in OA pathogenies and identify novel therapeutic targets for OA treatment.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fosfopiruvato Hidratase
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Apoptose
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Condrócitos
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Proteínas Supressoras de Tumor
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Proteínas de Ligação a DNA
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Matriz Extracelular
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Interleucina-1beta
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Inflamação
Limite:
Humans
Idioma:
En
Revista:
Tissue Cell
Ano de publicação:
2024
Tipo de documento:
Article
País de publicação:
Reino Unido