Microglia-specific deletion of histone deacetylase 3 promotes inflammation resolution, white matter integrity, and functional recovery in a mouse model of traumatic brain injury.

ABSTRACT:

Background

Histone deacetylases (HDACs) are believed to exacerbate traumatic brain injury (TBI) based on studies using pan-HDAC inhibitors. However, the HDAC isoform responsible for the detrimental effects and the cell types involved remain unknown, which may hinder the development of specific targeting strategies that boost therapeutic efficacy while minimizing side effects. Microglia are important mediators of post-TBI neuroinflammation and critically impact TBI outcome. HDAC3 was reported to be essential to the inflammatory program of in vitro cultured macrophages, but its role in microglia and in the post-TBI brain has not been investigated in vivo.

Methods

We generated HDAC3^LoxP mice and crossed them with CX3CR1^CreER mice, enabling in vivo conditio

SUBMITTER: Zhao Y 

PROVIDER: S-EPMC9357327 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature