神经突
原肌球蛋白受体激酶A
神经生长因子
神经营养素
医学
脊髓
神经营养因子
原肌球蛋白受体激酶B
神经保护
神经科学
脊髓损伤
星形胶质细胞
中枢神经系统
生物
体外
受体
内科学
生物化学
作者
Kei Ando,Shiro Imagama,Zenya Ito,Kazuyoshi Kobayashi,Takeyuki Hida,Hiroaki Nakashima,Kenyu Ito,Mikito Tsushima,Yoshimoto Ishikawa,Akiyuki Matsumoto,Kohji Nishida,Yoshihiro Nishida,Naoki Ishiguro
出处
期刊:Spine
[Ovid Technologies (Wolters Kluwer)]
日期:2016-04-22
卷期号:41 (20): E1201-E1207
被引量:18
标识
DOI:10.1097/brs.0000000000001611
摘要
Study Design. Self-assembling peptide gel (SPG-178) provides new evidence for the role of a scaffold for treatment of the spinal cord through induction of neuroprotective factors. Objective. To verify the reproducibility of SPG-178 as scaffold after spinal cord injury, we examine the characteristics of SPG-178 and protective effect on neural cells in vitro and in vivo . Summary of Background Data. The central nervous system extracellular matrix may play a role in maintenance of the neuronal network by inhibiting axonal growth and suppressing formation of additional inadequate synapses. In this study, we show increased expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT-4), and tropomyosin receptor kinase (TrkA and TrkB) in SPG-178-promoted neurite outgrowth of motor neurons in vitro , and decreased inflammation and glial scar with use of SPG-178 in vivo . Methods. We examined the effect of a self-assembling peptide, SPG-178, as a scaffold for neurite outgrowth of spinal motor neurons in vitro . An in vivo analysis was performed to evaluate if the SPG-178 scaffold attenuated or enhanced expression of various genes after spinal cord injury model rats. Results. Expression of NGF, BDNF, NT-4, TrkA, and TrkB increased in SPG-178-promoted neurite outgrowth of motor neurons in vitro . In vivo , SPG-178 increased expression of glial cell line-derived neurotrophic factor and NGF, and decreased glial scar. Conclusion. This study provides new evidence for the role of SPG-178 as a scaffold in the spinal cord and suggests that this peptide is a neuroprotective factor that may serve as an alternative treatment for neuronal injuries. Level of Evidence: 5
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