Regulation of inflammation and apoptosis by GPR43 via JNK/ELK1 in acute lung injury.
Inflamm Res
; 71(5-6): 603-614, 2022 Jun.
Article
em En
| MEDLINE
| ID: mdl-35306578
ABSTRACT
Acute lung injury (ALI) is mostly relevant to acute and severe lung inflammation. We first utilized lipopolysaccharide (LPS) to induce mice for establishing a mouse model of ALI and detected decreased expression of GPR43 in the lung tissue in mice with ALI. Mice expressing increased GPR43 showed improvement in lung injury compared to LPS-treated mice. Additionally, ALI mice transfected with lenti-GPR43 significantly decreased the mRNA levels of TNF-α, IL-1ß, IL-6, MPO, COX2 and iNOS, and apoptosis levels in the lungs, as well as the phosphorylation levels of JNK and ELK1 compared to LPS-treated mice with lenti-vector infection. Subsequently, we employed LPS to induce alveolar type ii epithelial cells and observed that Ov-GPR43 infection markedly reduced the expression levels of inflammatory factors and apoptosis levels, while exposure of cells to anisomycin was also effective in blunting the effects of Ov-GPR43 on these processes. Taken together, these results demonstrate a role of GPR43 in mediating lung injury through JNK/ELK1 and imply the therapeutic potential of targeting GPR43 against ALI.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Lipopolissacarídeos
/
Lesão Pulmonar Aguda
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article