ERK1/2-Mediated Schwann Cell Proliferation in the Regenerating Sciatic Nerve by Treadmill Training
Male
0301 basic medicine
0303 health sciences
Mitogen-Activated Protein Kinase 3
Proto-Oncogene Proteins c-jun
Growth Cones
Denervation
Exercise Therapy
Nerve Regeneration
Rats
Enzyme Activation
Rats, Sprague-Dawley
Disease Models, Animal
03 medical and health sciences
GAP-43 Protein
Ganglia, Spinal
Physical Conditioning, Animal
Exercise Test
Neurites
Animals
RNA, Messenger
Enzyme Inhibitors
Cell Proliferation
DOI:
10.1089/neu.2008.0711
Publication Date:
2009-10-15T18:33:31Z
AUTHORS (8)
ABSTRACT
Proliferation of Schwann cells in the injured peripheral nerve supports axonal regeneration, and physical training in experimental animals has been shown to promote nerve regeneration. Extracellular signal-regulated kinase 1/2 (ERK1/2) activity can mediate neuronal responses to lesion signals, but its role in non-neuronal cells in the injured area is largely unknown. Here we report that treadmill training (TMT) facilitates axonal regeneration via the upregulation of phospho-ERK1/2 protein levels in Schwann cells in the injured sciatic nerve. Low-intensity, but not high-intensity, TMT increased neurite outgrowth of dorsal root ganglion (DRG) sensory neurons and potentiated Schwann cell proliferation. TMT elevated levels of GAP-43 mRNA and protein, and phospho-ERK1/2 protein in the injured sciatic nerves. TMT also enhanced phospho-c-Jun protein levels in the injured nerve. In-vivo administration of the ERK1/2 inhibitor PD98059 eliminated phospho-c-Jun, suggesting ERK1/2 phosphorylation of the c-Jun protein. PD98059 treatment decreased levels of BrdU-labeled proliferating Schwann cells in the distal portion of the injured nerve, and delayed the axonal regrowth that was promoted by TMT. The present data suggest that increased ERK1/2 activity in Schwann cells may play an important role in TMT-mediated enhancement of axonal regeneration in the injured peripheral nerve.
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