Inhibition of CSPG receptor PTPσ promotes migration of newly born neuroblasts, axonal sprouting, and recovery from stroke.

Inhibition of CSPG receptor PTPσ promotes migration of newly born neuroblasts, axonal sprouting, and recovery from stroke.
复制标题

DOI:
10.1016/j.celrep.2022.111137
复制
发表时间:
2022-07-26
期刊:
影响因子:
8.8
通讯作者:
Luo, Yu
Luo, Yu
中科院分区:
生物学1区
文献类型:
--
作者:
Luo, Fucheng;Wang, Jiapeng;Zhang, Zhen;You, Zhen;Bedolla, Alicia;Okwubido-Williams, Feargod;Huang, L. Frank;Silver, Jerry;Luo, Yu

文献摘要

参考文献

被引文献

相似文献

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. ECM molecules called chondroitin sulfate proteoglycans are barriers to axonal plasticity and precursor cell migration after stroke. Luo et al. use a peptide to block PTPσ, a receptor that mediates the inhibition. Peptide treatment results in significant behavioral recovery accompanied by neuroprotection, axonal sprouting, and neuroblast migration into the lesion.
DOI: 10.1016/j.pneurobio.2016.03.009
发表时间: 2016-09
影响因子: 6.7
作者:
Filous AR;Silver J
通讯作者: Silver J
DOI: 10.1093/bioinformatics/btu638
发表时间: 2015-01-15
期刊: Bioinformatics (Oxford, England)
影响因子: --
作者:
Anders S;Pyl PT;Huber W
通讯作者: Huber W
DOI: 10.1186/s12974-018-1128-2
发表时间: 2018-03-20
影响因子: 9.3
作者:
Dyck S;Kataria H;Alizadeh A;Santhosh KT;Lang B;Silver J;Karimi-Abdolrezaee S
通讯作者: Karimi-Abdolrezaee S
DOI: 10.1093/brain/awy158
发表时间: 2018-08-01
期刊: Brain : a journal of neurology
影响因子: --
作者:
Burnside ER;De Winter F;Didangelos A;James ND;Andreica EC;Layard-Horsfall H;Muir EM;Verhaagen J;Bradbury EJ
通讯作者: Bradbury EJ
DOI: 10.1046/j.1471-4159.2003.02022.x
发表时间: 2003-11-01
影响因子: 4.7
作者:
Dempsey, RJ;Sailor, KA;Vemuganti, R
通讯作者: Vemuganti, R