β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38

Hui Yan, Hui Li, James Denney, Christopher Daniels, Krishna Singh, Balvin Chua, Charles Stuart, Yi Caudle, Ronald Hamdy, Gene LeSage, Deling Yin

Producción científica: Articlerevisión exhaustiva

3 Citas (Scopus)

Resumen

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.

Idioma originalEnglish (US)
Páginas (desde-hasta)130-137
Número de páginas8
PublicaciónBiochemistry and Biophysics Reports
Volumen7
DOI
EstadoPublished - sept 1 2016
Publicado de forma externa

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Cell Biology

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