Inhibiting Histone Deacetylase 2 (HDAC2) Promotes Functional Recovery From Stroke.

ABSTRACT: Stroke is a leading cause of long-term disability worldwide. However, current therapies that promote functional recovery from stroke are limited to physical rehabilitation. No pharmacological therapy is available. Thus, understanding the role of histone deacetylase 2 (HDAC2) in the pathophysiological process of stroke-induced functional loss may provide a novel strategy for stroke recovery. Focal stroke was induced by photothrombosis. LV-HDAC2-shRNA-GFP, LV-GFP, Ad-HDAC2-Flag, or Ad-inactive-HDAC2-Flag was microinjected into the peri-infarct area immediately after stroke. HDAC inhibitors were microinjected into the peri-infarct area 4 to 10 days after stroke. Grid-walking task and cylinder task were conducted to assess motor function. Golgi-Cox staining, chromatin immunoprecipitation, and

SUBMITTER: Tang Y 

PROVIDER: S-EPMC5721897 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature