ArticleCNS neuroscience & therapeutics2026
Inhibition of Transglutaminase 2 Preserves Blood-Brain Barrier Integrity and Improves Neurological Outcomes After Experimental Traumatic Brain Injury in Mice.
Article in CNS neuroscience & therapeutics, 2026. 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
backgroundTraumatic brain injury (TBI) is a leading global cause of disability and mortality, with blood-brain barrier (BBB) disruption exacerbating secondary injury. Transglutaminase 2 (TGM2), a multifunctional enzyme implicated in neuroinflammation and extracellular matrix remodeling, remains underexplored in TBI-related BBB dysfunction. This study elucidates the role of TGM2 in BBB disruption following TBI and explores its therapeutic potential in mitigating BBB damage.
methodsThe controlled cortical impact (CCI) and oxygen-glucose deprivation (OGD) models were used to establish in vivo and in vitro TBI models in mice. The experimental approaches comprised RNA sequencing, Western blot analysis, RT-qPCR, immunofluorescence staining, and behavioral assessments.
resultsTGM2 expression peaked at 48 h after TBI, predominantly in brain endothelial cells, correlating with BBB disruption (reduced tight junction proteins, increased edema). TGM2 knockdown may attenuate MMP-9 via the IL-17 pathway, restoring BBB integrity. In vivo, TGM2 inhibition reduced Evans blue leakage, upregulated CLAUDIN-5/ZO-1, and improved motor coordination, balance, and spatial memory.
conclusionTGM2 is a key molecule affecting the BBB after TBI. Inhibition of TGM2 can alleviate the blood-brain barrier and neurological deficits after TBI, acting through the IL-17-MMP-9 axis.
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