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The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

SOCS3 Deletion Promotes Optic Nerve Regeneration In Vivo

Open access
Smith, Patrice D., Sun, Fang, Park, Kevin Kyungsuk, Cai, Bin, Wang, Chen, Kuwako, Kenichiro, Martinez-Carrasco, Irene, Connolly, Lauren, He, Zhigang·2009·Neuron

Abstract

SUMMARY Axon regeneration failure accounts for permanent functional deficits following CNS injury in adult mammals. However, the underlying mechanisms remain elusive. In analyzing axon regeneration in different mutant mouse lines, we discovered that deletion of suppressor of cytokine signaling 3 (SOCS3), in adult retinal ganglion cells (RGCs), promotes robust regeneration of injured optic nerve axons. This regeneration-promoting effect is efficiently blocked in SOCS3-gp130 double knockout mice, suggesting that SOCS3 deletion promotes axon regeneration via a gp130-dependent pathway. Consistently, a transient up-regulation of ciliary neurotrophic factor (CNTF) was observed within the retina following optic nerve injury. Intravitreal application of CNTF further enhances axon regeneration from SOCS3-deleted RGCs. Together, our results suggest that compromised responsiveness to injury-induced growth factors in mature neurons contributes significantly to regeneration failure. Thus, developing strategies to modulate negative signaling regulators may be an efficient strategy of promoting axon regeneration after CNS injury.

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Crossref · 10.1016/j.neuron.2009.11.021

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Metadata

Authors
Smith, P. D., Sun, F., Park, K. K., Cai, B., Wang, C., Kuwako, K., Martinez-Carrasco, I., Connolly, L., & He, Z.
Venue
Neuron
Publisher
Elsevier BV
Published
2009-12
Volume
64
Issue
5
Pages
617-623
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2066858330
Cited by
502
References
4
FWCI
9.16
Type
journal article
Language
en
Open access
bronze

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