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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Park C,Cho IH,Kim D,Jo EK,Choi SY,Oh SB,Park K,Kim JS,Lee SJdoi
10.1016/j.neulet.2007.11.057subject
Has Abstractpub_date
2008-01-31 00:00:00pages
123-8issue
2eissn
0304-3940issn
1872-7972pii
S0304-3940(07)01214-1journal_volume
431pub_type
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