ß-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.
Biochem Biophys Rep
; 7: 130-137, 2016 Sep.
Article
em En
| MEDLINE
| ID: mdl-27957549
ABSTRACT
Sepsis is an exaggerated systemic inflammatory response to persistent bacteria infection with high morbidity and mortality rate clinically. ß-arrestin 2 modulates cell survival and cell death in different systems. However, the effect of ß-arrestin 2 on sepsis-induced cardiac dysfunction is not yet known. Here, we show that ß-arrestin 2 overexpression significantly enhances animal survival following cecal ligation and puncture (CLP)-induced sepsis. Importantly, overexpression of ß-arrestin 2 in mice prevents CLP-induced cardiac dysfunction. Also, ß-arrestin 2 overexpression dramatically attenuates CLP-induced myocardial gp130 and p38 mitogen-activated protein kinase (MAPK) phosphorylation levels following CLP. Therefore, ß-arrestin 2 prevents CLP-induced cardiac dysfunction through gp130 and p38. These results suggest that modulation of ß-arrestin 2 might provide a novel therapeutic approach to prevent cardiac dysfunction in patients with sepsis.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Biochem Biophys Rep
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
Estados Unidos