Injury-Induced Decline of Intrinsic Regenerative Ability Revealed by Quantitative Proteomics

Stephane Belin, Homaira Nawabi, Chen Wang, Shaojun Tang, Alban Latremoliere, Peter Warren, Hubert Schorle, Ceren Uncu, Clifford J. Woolf, Zhigang He, Judith A. Steen

Research output: Contribution to journalArticlepeer-review


Neurons differ in their responses to injury, but the underlying mechanisms remain poorly understood. Using quantitative proteomics, we characterized the injury-triggered response from purified intact and axotomized retinal ganglion cells (RGCs). Subsequent informatics analyses revealed a network of injury-response signaling hubs. In addition to confirming known players, such as mTOR, this also identified new candidates, such as c- myc, NFκB, and Huntingtin. Similar to mTOR, c- myc has been implicated as a key regulator of anabolic metabolism and is downregulated by axotomy. Forced expression of c- myc in RGCs, either before or after injury, promotes dramatic RGC survival and axon regeneration after optic nerve injury. Finally, in contrast to RGCs, neither c- myc nor mTOR was downregulated in injured peripheral sensory neurons. Our studies suggest that c- myc and other injury-responsive pathways are critical to the intrinsic regenerative mechanisms and might represent a novel target for developing neural repair strategies in adults.

Original languageEnglish (US)
Pages (from-to)1000-1014
Number of pages15
Issue number4
StatePublished - May 20 2015

ASJC Scopus subject areas

  • Neuroscience(all)

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