Genetic deletion of G protein-coupled receptor 56 aggravates traumatic brain injury through the microglial CCL3/4/5 upregulation targeted to CCR5.

ABSTRACT: Traumatic brain injury (TBI) is a significant global health concern that often results in death or disability, and effective pharmacological treatments are lacking. G protein-coupled receptor 56 (GPR56), a potential drug target, is crucial for neuronal and glial cell function and therefore plays important roles in various neurological diseases. Here, we investigated the potential role and mechanism of GPR56 in TBI-related damage to gain new insights into the pharmacological treatment of TBI. Our study revealed that TBI caused a significant decrease in GPR56 expression and that the deletion of Gpr56 exacerbated neurological function deficits and blood‒brain barrier (BBB) damage following TBI. Additionally, Gpr56 deletion led to increased microgliosis, increased infiltration of peripheral T

SUBMITTER: Sha Z 

PROVIDER: S-EPMC11910551 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature