Journal ArticleDOI
Advances in peripheral nerve regeneration
Jami L. Scheib,Ahmet Hoke +1 more
TLDR
Use of rodent models of chronic denervation will facilitate the understanding of the molecular mechanisms of peripheral nerve regeneration and create the potential to test therapeutic advances.Abstract:
Rodent models of nerve injury have increased our understanding of peripheral nerve regeneration, but clinical applications have been scarce, partly because such models do not adequately recapitulate the situation in humans. In human injuries, axons are often required to extend over much longer distances than in mice, and injury leaves distal nerve fibres and target tissues without axonal contact for extended amounts of time. Distal Schwann cells undergo atrophy owing to the lack of contact with proximal neurons, which results in reduced expression of neurotrophic growth factors, changes in the extracellular matrix and loss of Schwann cell basal lamina, all of which hamper axonal extension. Furthermore, atrophy and denervation-related changes in target tissues make good functional recovery difficult to achieve even when axons regenerate all the way to the target tissue. To improve functional outcomes in humans, strategies to increase the speed of axonal growth, maintain Schwann cells in a healthy, repair-capable state and keep target tissues receptive to reinnervation are needed. Use of rodent models of chronic denervation will facilitate our understanding of the molecular mechanisms of peripheral nerve regeneration and create the potential to test therapeutic advances.read more
Citations
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Journal ArticleDOI
The repair Schwann cell and its function in regenerating nerves
Kristjan R. Jessen,Rhona Mirsky +1 more
TL;DR: The transcription factor c‐Jun, although not required for Schwann cell development, is therefore central to the reprogramming of myelin and non‐myelin (Remak) Schwann cells to repair cells after injury.
Journal ArticleDOI
Peripheral nerve regeneration: Experimental strategies and future perspectives
TL;DR: This review summarises all the events occurring after nerve damage at the level of the cell body, the site of injury and the target organ.
Journal ArticleDOI
Bioactive polymeric scaffolds for tissue engineering.
Scott Stratton,Namdev B. Shelke,Kazunori Hoshino,Swetha Rudraiah,Sangamesh G. Kumbar,Sangamesh G. Kumbar +5 more
TL;DR: 3D scaffold fabrication methodologies with a focus on optimizing scaffold performance through the matrix pores, bioactivity and degradation rate to enable tissue regeneration are highlighted.
Journal ArticleDOI
The Success and Failure of the Schwann Cell Response to Nerve Injury.
Kristjan R. Jessen,Rhona Mirsky +1 more
TL;DR: The re-programming of Remak and myelin cells to repair cells, together with the injury-induced switch of peripheral neurons to a growth mode, gives peripheral nerves their strong regenerative potential.
Journal ArticleDOI
Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves
TL;DR: The emerging similarities between the injury response seen in nerves and in other tissues are discussed and the transcription factors, epigenetic mechanisms, and signaling cascades that control repair Schwann cells are surveyed, with emphasis on systems that selectively regulate the Schwann cell injury response.
References
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Journal ArticleDOI
Peripheral nerve regeneration
TL;DR: The presence of synaptic vesicle-associated proteins such as synaptophysin, synaptotagmin and synapsin I in the growth cones of regenerating axons indicates the possibility that exocytotic fusion of vesicles with the surface axolemma supplies the membranous components for the extension of regenerates axons.
Journal ArticleDOI
dSarm/Sarm1 Is Required for Activation of an Injury-Induced Axon Death Pathway
Jeannette M. Osterloh,Jing Yang,Timothy M. Rooney,A. Nicole Fox,Robert Adalbert,Eric Powell,Amy E. Sheehan,Michelle A. Avery,Rachel Hackett,Mary A. Logan,Jennifer M. MacDonald,Jennifer S. Ziegenfuss,Stefan Milde,Ying-Ju Hou,Carl Nathan,Aihao Ding,Robert H. Brown,Laura Conforti,Michael P. Coleman,Marc Tessier-Lavigne,Stephan Züchner,Marc R. Freeman +21 more
TL;DR: It is shown that loss of the Drosophila Toll receptor adaptor dSarm cell-autonomously suppresses Wallerian degeneration for weeks after axotomy, providing direct evidence that axons actively promote their own destruction after injury and identify dSARM/Sarm1 as a member of an ancient axon death signaling pathway.
Journal ArticleDOI
Control of mitochondrial motility and distribution by the calcium signal: a homeostatic circuit
TL;DR: Diminished mitochondrial motility in the region of the [Ca2+]c rise promotes recruitment of mitochondria to enhance local Ca2+ buffering and energy supply, which may provide a novel homeostatic circuit in calcium signaling.
Journal ArticleDOI
Why is Wallerian degeneration in the CNS so slow
Mauricio E. Vargas,Ben A. Barres +1 more
TL;DR: Current work on the mechanisms of WD is reviewed with an emphasis on deciphering this mystery and on understanding whether slow WD in the CNS could account for the failure of CNS axons to regenerate.
Journal ArticleDOI
Axoplasmic importins enable retrograde injury signaling in lesioned nerve
Shlomit Hanz,Eran Perlson,Dianna E. Willis,Jun-Qi Zheng,Rada Massarwa,Juan J. Huerta,Martin Koltzenburg,Matthias Köhler,Jan van-Minnen,Jeffery L. Twiss,Mike Fainzilber +10 more
TL;DR: A model whereby lesion-induced upregulation of axonal importin beta may enable retrograde transport of signals that modulate the regeneration of injured neurons is suggested.
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