Cd47 deficiency in mouse brain under excitotoxic stress.

Cd47 knockout in mouse hippocampus shifts single-nucleus transcriptome co-expression, with vehicle-treated KO cells most closely resembling wild-type cells exposed to KA3 (3 mg/kg), among 15 comparisons.

• Why it matters: It addresses how Cd47 influences neuronal stress and injury, filling a gap in linking its presynaptic abundance to excitotoxic response programs.
• What they did: Hippocampi from WT and Cd47 KO mice were profiled by single-nucleus RNA sequencing after kainic acid at KA25 (25 mg/kg) or KA3 (3 mg/kg), then analyzed with cell-type annotation plus WGCNA and Wasserstein-distance transcriptome comparisons.
• The result: KA-associated co-expression changes appeared only in Cd47-deficient cells for specific modules, enriched for translational, bioenergetic, and synaptic gene sets, suggesting Cd47 loss biases toward a mild excitotoxic-like state.

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