ArticleMolecular neurobiology2025
Ccn1 Mediates Pyroptosis and Purine Metabolism Pattern Shifts in a High-Uric Acid Microenvironment After Spinal Cord Injury.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Spinal cord injury (SCI) often results in permanent functional loss due to the complexity of the post-SCI microenvironment, but the composition and functional dynamics of the post-SCI microenvironment remain poorly understood. We applied spatial metabolomics to detect metabolites within the spinal cord of SCI rats, revealing the existence of a high-uric acid (hUA) microenvironment. Subsequently, we utilized Bulk-RNA sequencing and single-cell RNA sequencing (scRNA-seq) analysis, identified elevated expression of Cellular communication network factor 1 (Ccn1) and alterations in purine metabolic patterns. To investigate the role of Ccn1 within this hUA microenvironment, PC12 cell line and Sprague-Dawley (SD) rats were used. In vitro, 4 groups were designed: Control (n = 6), UA (PC12 cells treated with 200 μM UA for 24 h) (n = 6), siCcn1 (Ccn1 knockdown using small interfering RNA) (n = 6), and siCcn1 + UA (n = 6). In vivo groups: SCI (spinal cord injury only) (n = 6), hUA (induced hUA microenvironment by gavage with oxonic acid potassium salt 750 mg/kg and and ethambutol 250 mg/kg) (n = 6), AAV (Ccn1 knockdown via adeno-associated virus) (n = 6), and AAV + hUA (n = 6). Results showed that UA significantly reduced cellular aerobic respiration levels (Control vs UA: 62.87 ± 16.76 vs 17.09 ± 4.91 pmol/min, P < 0.01) and induced pyroptosis, Ccn1 knockdown significantly improved aerobic respiration (siCcn1 + UA vs UA: 46.45 ± 12.54 vs 17.09 ± 4.91 pmol/min, P < 0.05) and reduced the level of pyroptosis. Total cellular ATP levels, the NAD⁺/NADH ratio, and proliferation capacity were also assessed. In vivo, Ccn1 knockdown significantly increased the Basso, Beattie, and Bresnahan (BBB) locomotor scores of animals on the 7 days post-injury (AAV + hUA vs hUA: 3.33 ± 0.52 vs 2.00 ± 0.63, P < 0.05) and reduced neuronal pyroptosis. The hUA microenvironment upregulated Ccn1 expression, suppressed aerobic respiration, induced pyroptosis, and disrupted purine metabolism, Ccn1 knockdown reversed these biological processes, suggesting its potential as a therapeutic target for SCI.
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