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ABSTRACT: Background
Deficient DNA repair and excessive DNA damage contribute to neurodegenerative disease. However, the role of DNA damage and repair in spinal cord injury (SCI) is unclear. SCI, a debilitating disruption of the structural and biological network of the spinal cord, is characterized by oxidative stress. Nevertheless, the pathophysiological mechanisms leading to neuronal loss following SCI remain incompletely defined.Methods
Using a contusion model, a severe SCI was induced at the L1 spinal level in C57Bl/6J mice. The temporal and spatial presence of DNA damage was then determined via immunolabeling for the DNA damage marker, γH2AX, from 1 h post-injury (hpi) to 28 days post-injury (dpi).Results
Our analysis revealed that increased DNA damage foci were present
SUBMITTER: Scheijen EE
PROVIDER: S-EPMC11756142 | biostudies-literature | 2025 Jan
REPOSITORIES: biostudies-literature