Fibroblast growth factor 21 protects against pathological cardiac remodeling by modulating galectin-3 expression.
J Cell Biochem
; 120(12): 19529-19540, 2019 12.
Article
em En
| MEDLINE
| ID: mdl-31286550
ABSTRACT
BACKGROUND/AIMS:
Fibroblast growth factor 21 (FGF21) plays a protective role in ischemia/reperfusion induced cardiac injury. However, the exact molecular mechanism of FGF21 action remains unclear. This study was designed the protective effect of FGF21 on the heart and its mechanism.METHOD:
Adenovirus vector expressing FGF21 or control ß-galactosidase was injected into the myocardium of mice. Myocardial injury was observed by tissue staining and immunohistochemical staining. The expression level of caspases-3 and galectin-3 in myocardial cells were observed by immunoblotting. Then, hypoxia-induced cell model was established. Small interfering RNA (SiRNA) and plasmid were transfected into H9c2 using Lipofectamine 2000 reagent (Invitrogen). The expression levels of galectin-3, ECM and cystatin-3 in cells were observed by immunoblotting, and the relationship between fibroblast growth factor 21 and galectin-3 was analyzed.RESULT:
Cell test in vitro showed that FGF21 could inhibit apoptosis and decrease the expression of ECM (ColIaI, fibronectin, and alpha-SMA) under hypoxia. Western blot data showed that hypoxia-induced cell damage increased galectin-3 levels, while FGF21 decreased galactose lectin-3 levels. In addition, inhibition of galactose agglutinin-3 expression by siRNA enhanced the cardioprotective effect of FGF21, while overexpression of galectin-3 reduced the cardioprotective effect of fibroblast growth factor 21.CONCLUSION:
FGF21 may be a novel therapy for hypoxia-induced cardiac injury by regulating the expression of galectin-3.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Fibrose
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Traumatismo por Reperfusão
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Isquemia Miocárdica
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Substâncias Protetoras
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Miócitos Cardíacos
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Galectina 3
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Fatores de Crescimento de Fibroblastos
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article