C3aR signaling and gliosis in response to neurodevelopmental damage in the cerebellum.

ABSTRACT:

Background

Conditional ablation of the Smarca5 gene in mice severely impairs the postnatal growth of the cerebellum and causes an ataxic phenotype. Comparative gene expression studies indicated that complement-related proteins were upregulated in the cerebellum of Smarca5 mutant mice. Complement proteins play critical roles within innate immune signaling pathways and, in the brain, are produced by glial cells under both normal and pathological conditions. The C3 complement protein-derived signaling peptide, C3a, has been implicated in contributing to both tissue damage and repair in conditions such as multiple sclerosis and stroke. Here, we investigated whether C3a receptor (C3aR) signaling promoted damage or repair in the developing cerebellum of Smarca5 mutant mice.

Methods

SUBMITTER: Young KG 

PROVIDER: S-EPMC6610970 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature