神经母细胞
硫酸软骨蛋白多糖
神经保护
神经突
神经科学
下调和上调
神经退行性变
冲程(发动机)
神经发生
神经干细胞
轴突
细胞生物学
抑制性突触后电位
生物
蛋白多糖
医学
细胞外基质
干细胞
内科学
生物化学
基因
机械工程
工程类
疾病
体外
作者
Fucheng Luo,Jiapeng Wang,Zhen Zhang,Zhen You,Alicia Bedolla,FearGod V Okwubido-Williams,L. Frank Huang,Jerry Silver,Yu Luo
出处
期刊:Cell Reports
[Elsevier]
日期:2022-07-01
卷期号:40 (4): 111137-111137
被引量:21
标识
DOI:10.1016/j.celrep.2022.111137
摘要
In addition to neuroprotective strategies, neuroregenerative processes could provide targets for stroke recovery. However, the upregulation of inhibitory chondroitin sulfate proteoglycans (CSPGs) impedes innate regenerative efforts. Here, we examine the regulatory role of PTPσ (a major proteoglycan receptor) in dampening post-stroke recovery. Use of a receptor modulatory peptide (ISP) or Ptprs gene deletion leads to increased neurite outgrowth and enhanced NSCs migration upon inhibitory CSPG substrates. Post-stroke ISP treatment results in increased axonal sprouting as well as neuroblast migration deeply into the lesion scar with a transcriptional signature reflective of repair. Lastly, peptide treatment post-stroke (initiated acutely or more chronically at 7 days) results in improved behavioral recovery in both motor and cognitive functions. Therefore, we propose that CSPGs induced by stroke play a predominant role in the regulation of neural repair and that blocking CSPG signaling pathways will lead to enhanced neurorepair and functional recovery in stroke.
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