Document Type
Article
Publication Date
9-1-2016
Description
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.
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Citation Information
Yan, Hui; Li, Hui; Denney, James; Daniels, Christopher; Singh, Krishna; Chua, Balvin; Stuart, Charles; Caudle, Yi; Hamdy, Ronald; LeSage, Gene; and Yin, Deling. 2016. β-arrestin 2 Attenuates Cardiac Dysfunction in Polymicrobial Sepsis Through gp130 and p38. Biochemistry and Biophysics Reports. Vol.7 130-137. https://doi.org/10.1016/j.bbrep.2016.05.021
Copyright Statement
c 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).