Chd8 Rescued TBI-Induced Neurological Deficits by Suppressing Apoptosis and Autophagy Via Wnt Signaling Pathway.

ABSTRACT: Traumatic brain injury (TBI) and autism spectrum disorder (ASDs) share several same biochemical mechanisms and symptoms, such as learning memory impairments and communication deficits. Chromodomain helicase DNA binding protein 8 (CHD8), a member of the CHD family of ATP-dependent chromatin remodeling factors, is one of the top risk genetic factors in ASDs and is highly associated with Wnt/β-catenin signaling. Yet, the possible effect of CHD8 on TBI remains poorly understood. In vivo, we found that Chd8 co-localized in neurons, astrocytes, and microglia, but predominantly presented in neurons in the prefrontal cortex, hippocampus, and cortex. Both Chd8 and β-catenin expression peaked at 12 h and shared the similar change tendency after TBI. Chd8 knockdown inhibited wnt pathway, promoted the

SUBMITTER: Chen J 

PROVIDER: S-EPMC11448946 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature