A20 Ameliorates Intracerebral Hemorrhage-Induced Inflammatory Injury by Regulating TRAF6 Polyubiquitination.

ABSTRACT: Reducing excessive inflammation is beneficial for the recovery from intracerebral hemorrhage (ICH). Here, the roles and mechanisms of A20 (TNFAIP3), an important endogenous anti-inflammatory factor, are examined in ICH. A20 expression in the PBMCs of ICH patients and an ICH mouse model was detected, and the correlation between A20 expression and neurologic deficits was analyzed. A20 expression was increased in PBMCs and was negatively related to the modified Rankin Scale score. A20 expression was also increased in mouse perihematomal tissues. A20^-/- and A20-overexpressing mice were generated to further analyze A20 function. Compared with wild-type (WT) mice, A20^-/- and A20-overexpressing mice showed significant increases and decreases, respectively, in hematoma volume

SUBMITTER: Meng Z 

PROVIDER: S-EPMC5220121 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature