β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke.

ABSTRACT: BACKGROUND:Stroke-induced immunodeficiency syndrome (SIDS) is regarded as a protective mechanism for secondary inflammatory injury as well as a contributor to infection complications. Although stroke-induced hyperactivation of the sympathetic system is proved to facilitate SIDS, the involved endogenous factors and pathways are largely elusive. In this study, we aim to investigate the function of beta-arrestin-2 (ARRB2) in the sympathetic-mediated SIDS. METHODS:Splenic ARRB2 expression and the sympathetic system activity were detected after establishing transient models of middle cerebral artery occlusion (MCAO). In addition, a correlation between ARRB2 expression and the sympathetic system activity was analyzed using a linear correlation analysis. Any SIDS reflected in monocyte dysfunction

SUBMITTER: Wang H 

PROVIDER: S-EPMC5894164 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature