@techreport{oai:mie-u.repo.nii.ac.jp:00014502,
 author = {長谷川, 正裕 and Hasegawa, Masahiro and 須藤, 啓広 and Sudo, Akihiro and 吉田, 利通 and Yoshida, Toshimichi},
 month = {May},
 note = {application/pdf, テネイシンC(TNC)のドメインであるTNIIIA2の軟骨変性抑制作用を調べるために、マウスの靭帯切離による外傷性変形性関節症モデルを作製し、TNIIIA2を投与すると軟骨変性抑制効果を8週まで認め、関節炎の誘発も認めなかった。
培養軟骨細胞にTNIIIA2を添加して遺伝子発現の差異をreal-time PCRで解析すると、炎症性サイトカインであるTNFα、軟骨細胞のanabolic factor であるbFGF、catabolic factorであるMMP3の遺伝子発現量がコントロール群と比較し有意に多かった。, TNIIIA2 is a peptide of tenascin-C. We evaluated whether TNIIIA2 could prevant articular cartilage degeneration without inducing synovitis in vivo study. TNIIIA2 was injected into the knee joint of mice to evaluate the induction of synovitis. Synovitis was not enhanced with TNIII2 administration. TNIIIA2 was injected into the knee joint of post-traumatic osteoarthritis mice model. Histologic examinations were made. Development of osteoarthritis was suppressed.
An in vitro study was also performed using cultured human  chondrocytes. The expressions of various mRNA were compared with TNIIIA2 treatment using real-time polymerase chain reaction. TNIIIA2 upregulated the expressions of tumor necrosis factor-α, matrix metalloproteinase 3, and basic fibroblast growth factor. In conclusion, we demonstrated that YNIIIA2 coould prevent cartilage degeneration without synovitis., 2017年度～2019年度科学研究費補助金(基盤研究(C))研究成果報告書, 17K11003},
 title = {テネイシンＣのドメイン(TNIIIA2)を用いた軟骨治療への応用},
 year = {2020},
 yomi = {ハセガワ, マサヒロ and スドウ, アキヒロ and ヨシダ, トシミチ}
}