• Masato Shiba, Masashi Fujimoto, Fumio Kawakita, Kyoko Imanaka-Yoshida, Toshimichi Yoshida, Kenji Kanamaru, Waro Taki, and Hidenori Suzuki.
• Department of Neurosurgery, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan, mshiba@clin.medic.mie-u.ac.jp.
• Acta Neurochir. Suppl. 2015 Jan 1;120:69-73.

Background And PurposeWe previously reported that tenascin-C (TNC), a matricellular protein, was involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the role of TNC in early brain injury (EBI) is unknown. This study assessed whether inhibition of TNC upregulation in brain by imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of platelet-derived growth factor receptors, prevents EBI after experimental SAH.MethodsRats were assigned to sham, SAH plus vehicle, and SAH plus imatinib groups (n = 4 per group). Imatinib (50 mg/kg body weight) was administered intraperitoneally to rats undergoing SAH by endovascular perforation, and EBI was evaluated using terminal deoxynucleotidyl transferase-mediated uridine 5-triphosphate-biotin nick end-labeling staining at 24 h after SAH. Imatinib-treated SAH rats were also treated by a cisternal injection of recombinant TNC.ResultsSAH upregulated TNC and caused EBI. Imatinib treatment suppressed both TNC upregulation and EBI at 24 h. Recombinant TNC reinduced EBI in imatinib-treated SAH rats.ConclusionsTNC may be involved in the pathogenesis of EBI after SAH.

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