Toll-like receptor 2 contributes to glial cell activation and heme oxygenase-1 expression in traumatic brain injury |
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Authors: | Park Chanhee Cho Ik-Hyun Kim Donghoon Jo Eun-Kyeong Choi Se-Young Oh Seog Bae Park Kyoungpyo Kim Joong Soo Lee Sung Joong |
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Affiliation: | Program in Molecular and Cellular Neuroscience, DRI, and Department of Oral Physiology, School of Dentistry, Seoul National University, 28 Yeongun-dong, Jongno-gu, Seoul 110-749, Republic of Korea. |
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Abstract: | Traumatic brain injury is accompanied by glial cell activation around the site of the injury. In this study, we investigated the role of toll-like receptor 2 (TLR2) in glial cell activation using a stab-wound injury (SWI) model with TLR2 knock-out mice. Penetration of a normal mouse brain with a 26-G needle using a stereotaxic instrument resulted in an 18- and 4-fold upregulation of GFAP and CD11b mRNA, respectively, along the needle track in the injury area. However, in the TLR2 knock-out mice, the induced expression of these genes was reduced by 70% and 40%, respectively. Likewise, there was a reduction in the area of activated glial cells detected by immunohistochemistry and the glial cells had a less-activated morphology in the TLR2 knock-out mice. In addition, the expression of the heme oxygenase-1 (HO-1) gene, a glia-expressing wound-responsive gene, was reduced after SWI in TLR2 knock-out mice. Taken together, these data argue that TLR2 contributes to the glial cell activation and HO-1 gene expression associated with traumatic brain injury. |
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Keywords: | Toll-like receptor 2 Heme oxygenase-1 Glial activation Stab-wound injury |
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