Sugitani Kayo, Matsukawa Toru, Maeda Ari, Kato Satoru
Department of Molecular Neurobiology, Graduate School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8640, Japan.
Adv Exp Med Biol. 2006;572:525-30. doi: 10.1007/0-387-32442-9_73.
To elucidate the molecular involvement of transglutaminase (TG) in central nervous system (CNS) regeneration, we cloned a full-length cDNA for neural TG (TG(N)) from axotomized goldfish retinas and produced a recombinant TG(N) protein from this cDNA. The levels of TG(N) mRNA and protein were increased at 10-30 days after optic nerve transection, and this increase in TG(N) was only localized in the ganglion cells in goldfish retinas. In retinal explant cultures, the recombinant TG(N) protein induced a drastic enhancement of neurite outgrowth, while TG(N)-specific RNAi significantly suppressed this neurite outgrowth. Taken together, these data strongly indicate that TG(N) is a key regulatory molecule for CNS regeneration.
为阐明转谷氨酰胺酶(TG)在中枢神经系统(CNS)再生中的分子作用,我们从视神经切断的金鱼视网膜中克隆了神经TG(TG(N))的全长cDNA,并从该cDNA制备了重组TG(N)蛋白。视神经横断后10 - 30天,TG(N) mRNA和蛋白水平升高,且这种TG(N)的增加仅局限于金鱼视网膜的神经节细胞中。在视网膜外植体培养中,重组TG(N)蛋白显著促进了神经突生长,而TG(N)特异性RNA干扰则显著抑制了这种神经突生长。综上所述,这些数据有力地表明TG(N)是CNS再生的关键调节分子。