Abstract
Sepsis is an exaggerated systemic inflammatory response to persistent bacteria infection with high morbidity and mortality rate clinically. β-arrestin 2 modulates cell survival and cell death in different systems. However, the effect of β-arrestin 2 on sepsis-induced cardiac dysfunction is not yet known. Here, we show that β-arrestin 2 overexpression significantly enhances animal survival following cecal ligation and puncture (CLP)-induced sepsis. Importantly, overexpression of β-arrestin 2 in mice prevents CLP-induced cardiac dysfunction. Also, β-arrestin 2 overexpression dramatically attenuates CLP-induced myocardial gp130 and p38 mitogen-activated protein kinase (MAPK) phosphorylation levels following CLP. Therefore, β-arrestin 2 prevents CLP-induced cardiac dysfunction through gp130 and p38. These results suggest that modulation of β-arrestin 2 might provide a novel therapeutic approach to prevent cardiac dysfunction in patients with sepsis.
Original language | English (US) |
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Pages (from-to) | 130-137 |
Number of pages | 8 |
Journal | Biochemistry and Biophysics Reports |
Volume | 7 |
DOIs | |
State | Published - Sep 1 2016 |
Externally published | Yes |
Keywords
- Cardiac function
- Gp130
- P38
- Sepsis
- β-arrestin 2
ASJC Scopus subject areas
- Biophysics
- Biochemistry