title: Toll-like receptor 2 contributes to glial cell activation and heme oxygenase-1 expression in traumatic brain injury.
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.
authors.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.
authors.forename: Chanhee
authors.initials: C
authors.lastname: Park
authors.forename: Ik-Hyun
authors.initials: IH
authors.lastname: Cho
authors.forename: Donghoon
authors.initials: D
authors.lastname: Kim
authors.forename: Eun-Kyeong
authors.initials: EK
authors.lastname: Jo
authors.forename: Se-Young
authors.initials: SY
authors.lastname: Choi
authors.forename: Seog Bae
authors.initials: SB
authors.lastname: Oh
authors.forename: Kyoungpyo
authors.initials: K
authors.lastname: Park
authors.forename: Joong Soo
authors.initials: JS
authors.lastname: Kim
authors.forename: Sung Joong
authors.initials: SJ
authors.lastname: Lee
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D018845:CD11 Antigens / Q000235:genetics / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism*; D039001:Integrin alpha Chains / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008840:Microfilament Proteins; D009457:Neuroglia / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051195:Toll-Like Receptor 2 / Q000172:deficiency / Q000502:physiology*
chemical_list: C491049:Aif1 protein, mouse; D018845:CD11 Antigens; D002135:Calcium-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; D039001:Integrin alpha Chains; D008840:Microfilament Proteins; D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2; C527123:integrin alphaD, mouse; D051547:Heme Oxygenase-1