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NgR1 和 NgR3 是软骨素蛋白聚糖的受体。

NgR1 and NgR3 are receptors for chondroitin sulfate proteoglycans.

机构信息

Neuroscience Program, University of Michigan School of Medicine, Ann Arbor, Michigan, USA.

出版信息

Nat Neurosci. 2012 Mar 11;15(5):703-12. doi: 10.1038/nn.3070.

DOI:10.1038/nn.3070
PMID:22406547
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3337880/
Abstract

In the adult mammalian CNS, chondroitin sulfate proteoglycans (CSPGs) and myelin-associated inhibitors (MAIs) stabilize neuronal structure and restrict compensatory sprouting following injury. The Nogo receptor family members NgR1 and NgR2 bind to MAIs and have been implicated in neuronal inhibition. We found that NgR1 and NgR3 bind with high affinity to the glycosaminoglycan moiety of proteoglycans and participate in CSPG inhibition in cultured neurons. Nogo receptor triple mutants (Ngr1(-/-); Ngr2(-/-); Ngr3(-/-); which are also known as Rtn4r, Rtn4rl2 and Rtn4rl1, respectively), but not single mutants, showed enhanced axonal regeneration following retro-orbital optic nerve crush injury. The combined loss of Ngr1 and Ngr3 (Ngr1(-/-); Ngr3(-/-)), but not Ngr1 and Ngr2 (Ngr1(-/-); Ngr2(-/-)), was sufficient to mimic the triple mutant regeneration phenotype. Regeneration in Ngr1(-/-); Ngr3(-/-) mice was further enhanced by simultaneous ablation of Rptpσ (also known as Ptprs), a known CSPG receptor. Collectively, our results identify NgR1 and NgR3 as CSPG receptors, suggest that there is functional redundancy among CSPG receptors, and provide evidence for shared mechanisms of MAI and CSPG inhibition.

摘要

在成年哺乳动物中枢神经系统中，软骨素硫酸盐蛋白聚糖 (CSPGs) 和髓鞘相关抑制剂 (MAIs) 稳定神经元结构，并限制损伤后的代偿性发芽。Nogo 受体家族成员 NgR1 和 NgR2 与 MAIs 结合，并与神经元抑制有关。我们发现 NgR1 和 NgR3 与蛋白聚糖的糖胺聚糖部分具有高亲和力，并参与培养神经元中的 CSPG 抑制。Nogo 受体三重突变体（Ngr1(-/-); Ngr2(-/-); Ngr3(-/-)；分别也称为 Rtn4r、Rtn4rl2 和 Rtn4rl1），但不是单突变体，在眶后视神经挤压损伤后表现出增强的轴突再生。Ngr1 和 Ngr3 的联合缺失（Ngr1(-/-); Ngr3(-/-)），而不是 Ngr1 和 Ngr2（Ngr1(-/-); Ngr2(-/-)）足以模拟三重突变体的再生表型。Ngr1(-/-); Ngr3(-/-) 小鼠中的再生通过同时消融 Rptpσ（也称为 Ptprs）进一步增强，Rptpσ（也称为 Ptprs）是一种已知的 CSPG 受体。总的来说，我们的结果确定 NgR1 和 NgR3 为 CSPG 受体，表明 CSPG 受体之间存在功能冗余，并为 MAI 和 CSPG 抑制的共同机制提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/b7ee73bee3db/nihms357951f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/d76621186c60/nihms357951f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/ab9af6d0392b/nihms357951f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/d2765632ae9f/nihms357951f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/04d58d593dad/nihms357951f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/360745ede127/nihms357951f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/4776ac782d20/nihms357951f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/eeeb8bdb8f83/nihms357951f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/b7ee73bee3db/nihms357951f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/d76621186c60/nihms357951f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/ab9af6d0392b/nihms357951f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/d2765632ae9f/nihms357951f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/04d58d593dad/nihms357951f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/360745ede127/nihms357951f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/4776ac782d20/nihms357951f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/eeeb8bdb8f83/nihms357951f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1168/3337880/b7ee73bee3db/nihms357951f8.jpg

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