@article{oai:twinkle.repo.nii.ac.jp:00020466,
 author = {遠井, 素乃 and 柴田, 亮行 and 内山, 真一郎 and 岡田, 芳和 and 川俣, 貴一 and 川島, 明次 and 加藤, 陽一郎 and 澤田, 達男 and 小林, 槇雄 and 宇羽野, 惠 and 岩田, 誠},
 issue = {Extra},
 journal = {東京女子医科大学雑誌},
 month = {Feb},
 note = {神経内科学教室岩田誠教授退任記念特別号, Emerging evidence suggests that plaque destabilization based on persistent inflammation in carotid atherosclerosis (CAS) plays a critical role in cerebral infarction. Tissue factor (TF) acts as a membrane-bound receptor for activated factor VII triggering proinflammatory cell signaling. The aim of the present study was to determine the involvement of TF in destabilization of CAS plaques. This study was carried out on carotid endarterectomy specimens obtained from twenty CAS patients. The specimens were processed for making 30% sucroseimmersed, optimal cutting temperature (OCT) compound-embedded frozen sections and freshly frozen materials; the former was used for immunohistochemistry, and the latter for immunoblotting. The primary antibodies were mouse monoclonal IgG_1 against TF, CD68, α-smooth muscle actin (SMA), and β-actin. Immunoreaction on sections was visualized by the avidin-biotin-immunoperoxidase complex method, and that on blots was detected by the chemiilluminescence method. TF immunoreactivity was localized to endothelial cells, CD 68-immunoreactive macrophages, and SMA-immunoreactive smooth muscle cells, and it was prominent in macrophage-rich plaques (MRPs) compared with macrophage-poor plaques (MPPs). The immunoreactive density for TF normalized with β-actin was significantly increased in the MRP group compared with the MPP group. Our results suggest that TF participates in destabilization of CAS plaques, by its expression in the lesional cells.},
 pages = {E154--E159},
 title = {頸動脈アテローム硬化プラークにおける組織因子の発現(神経内科学教室岩田誠教授退任記念特別号)},
 volume = {78},
 year = {2008}
}