Functinal analysis of TGF-beta in the injured central nervous system

2014 Fiscal Year Final Research Report

• Project/Area Number: 23500422
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: Tokyo Metropolitan Institute of Medical Science
• Principal Investigator: KAWANO Hitoshi 公益財団法人東京都医学総合研究所, 脳発達・神経再生研究分野, 研究員 (20161341)
• Co-Investigator(Kenkyū-buntansha): KURODA Junko 公益財団法人東京都医学総合研究所, 脳発達・神経再生研究分野, 研究員 (20142151)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 神経再生 / 線維性瘢痕 / TGF-beta / コンドロイチン硫酸 / デルマタン硫酸

Outline of Final Research Achievements

The role of chondroitin sulfate (CS) and dermatan sulfate (DS) was examined in mice after transection of nigrostriatal dopaminergic pathway and treatment with of glycosaminoglycan degrading enzymes. Two weeks after injury, fibrotic and glial scars were formed around the lesion and transected axons did not regenerate beyond the lesion. Injection of chondroitinase B. which degrades DS, into the lesion site completely suppressed the fibrotic scar formation, reduced the glial scar and promoted the regeneration of dopaminergic axons. In contrast, injection of chondroitinase AC, a CS-degrading enzyme, did not suppress the fibrotic scar formation, but promoted the axonal regeneration. These results first demonstrate that DS and CS play different functions after CNS injury: DS is involved in the lesion scar formation and CS inhibits axonal regeneration (Li et al., 2013).

Free Research Field

神経再生