β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.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.
β-arrestin 2
β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.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.
β-arrestin 2
β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.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.
β-arrestin 2
β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.Sepsis is an exaggerated systemic inflammatory response to persistent bacteria infection with high morbidity and mortality rate clinically.  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. 
gp130 and p38
β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.Sepsis is an exaggerated systemic inflammatory response to persistent bacteria infection with high morbidity and mortality rate clinically.  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. 
gp130 and p38
β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.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.
β-arrestin 2