title: 3CB2, a marker of radial glia, expression after experimental intracerebral hemorrhage: role of thrombin.
abstract: The current study examined 3CB2, a marker of radial glia, expression after intracerebral hemorrhage (ICH) and intracerebral thrombin injection. Adult male Sprague-Dawley rats received an intracaudate injection of 100 microl autologous whole blood or 5 U thrombin (50 microl). Animals were sacrificed for Western blotting to quantify 3CB2 expression, and for single and double labeling immunohistochemistry to identify which cells express 3CB2. Behavioral examinations (forelimb placing test and corner turn test) were performed as an evaluation of function. By Western blot analysis, 3CB2 was strongly expressed at day 3 and the expression persisted for at least 1 month. Intracerebral injection of thrombin also upregulated 3CB2. Hirudin, a thrombin inhibitor, reduced ICH-induced 3CB2 expression. By immunohistochemistry, 3CB2 immunoreactivity was present in large numbers of glial cells surrounding the hematoma at 1 day after ICH. One month later, 3CB2 immunoreactivity was co-localized with a neuronal precursor marker, TUC-4. ICH-induced behavioral deficits were severe at 1, 3 and 7 days, with recovery at 1 month. The forelimb placing test score paralleled changes in 3CB2 expression. ICH-induced 3CB2 expression in glial cells may reflect an early response of these cells to injury, while the delayed expression in neurons might be a part of the adaptative response to injury perhaps participating in recovery of function. Thrombin has a role in 3CB2 expression in ICH.
authors.affiliation: Department of Neurobiology, Kagawa University Faculty of Medicine, Kagawa, Japan. tanakamu@kms.ac.jp
authors.forename: Takehiro
authors.initials: T
authors.lastname: Nakamura
authors.forename: Osamu
authors.initials: O
authors.lastname: Miyamoto
authors.forename: Tetsuhiko
authors.initials: T
authors.lastname: Toyoshima
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Hirooka
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Kawai
authors.forename: Fumio
authors.initials: F
authors.lastname: Shiraga
authors.forename: Takashi
authors.initials: T
authors.lastname: Tamiya
authors.forename: Guohua
authors.initials: G
authors.lastname: Xi
authors.forename: Richard F
authors.initials: RF
authors.lastname: Keep
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Itano
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002543:Cerebral Hemorrhage / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D005552:Forelimb / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000187:drug effects*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006490:Hemostatics / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013917:Thrombin / Q000494:pharmacology* / Q000627:therapeutic use; D013918:Thrombin Time; D013997:Time Factors; D014738:Vibrissae / Q000187:drug effects / Q000294:innervation; D014746:Vimentin / Q000378:metabolism*
chemical_list: C449760:Dpysl3 protein, rat; D005904:Glial Fibrillary Acidic Protein; D006490:Hemostatics; D009419:Nerve Tissue Proteins; D014746:Vimentin; D013917:Thrombin