Targeting cell surface receptors for axon regeneration in the central nervous system

• 作 者: Menghon Cheah Melissa R.Andrews
• 机 构: John van Geest Centre for Brain Repair,University of Cambridge,School of Medicine,University of St.A
• 出 处: Neural Regeneration Research
• 发表日期: 2016年12期
• 关键词: regeneration integrin neuronal neurotrophic extrinsic intrinsic chondroitin inju

Axon regeneration in the CNS is largely unsuccessful due to excess inhibitory extrinsic factors within lesion sites together with an intrinsic inability of neurons to regrow following injury. Recent work demonstrates that forced expression of certain neuronal transmembrane receptors can recapitulate neuronal growth resulting in successful growth within and through inhibitory lesion environments. More specifically, neuronal expression of integrin receptors such as alpha9beta1 integrin which binds the extracellular matrix glycoprotein tenascin-C, trk receptors such as trk B which binds the neurotrophic factor BDNF, and receptor PTPσ which binds chondroitin sulphate proteoglycans, have all been show to significantly enhance regeneration of injured axons. We discuss how reintroduction of these receptors in damaged neurons facilitates signalling from the internal environment of the cell with the external environment of the lesion milieu, effectively resulting in growth and repair following injury. In summary, we suggest an appropriate balance of intrinsic and extrinsic factors are required to obtain substantial axon regeneration.

Axon regeneration in the CNS is largely unsuccessful due to excess inhibitory extrinsic factors within lesion sites together with an intrinsic inability of neurons to regrow following injury. Recent work demonstrates that forced expression of certain neuronal transmembrane receptors can recapitulate neuronal growth resulting in successful growth within and through inhibitory lesion environments. More specifically, neuronal expression of integrin receptors such as alpha9beta1 integrin which binds the extracellular matrix glycoprotein tenascin-C, trk receptors such as trk B which binds the neurotrophic factor BDNF, and receptor PTPσ which binds chondroitin sulphate proteoglycans, have all been show to significant enhance regeneration of injured axons. We discuss how reintroduction of these receptors in damaged neurons facilitates signaling from the internal environment of the cell with the external environment of the lesion milieu, efficiently resulting in growth and repair following In summary, we suggest an appropriate balance of intrinsic and extrinsic factors are required to obtain a substantial axon regeneration.