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The Journal of Neuroscience, November 15, 2002, 22(22):9831-9840
A Novel Cytokine Pathway Suppresses Glial Cell Melanogenesis
after Injury to Adult Nerve
Tilat A.
Rizvi1,
Yuan
Huang1,
Amer
Sidani1,
Radhika
Atit1,
David A.
Largaespada3,
Raymond E.
Boissy2, and
Nancy
Ratner1
Departments of 1 Cell Biology, Neurobiology, and
Anatomy and 2 Dermatology, University of Cincinnati,
College of Medicine, Cincinnati, Ohio 45267-0521, and
3 Department of Genetics, University of Minnesota Cancer
Center, Minneapolis, Minnesota 55455
The neural crest gives rise to numerous cell types, including
Schwann cells, neurons, and melanocytes. The extent to which adult
neural crest-derived cells retain plasticity has not been tested
previously. We report that cutting adult mouse sciatic nerve induces
pigmentation around nerve fascicles, among muscle bundles, and in the
hypodermis. Pigmented cells are derived from adult nerve, because
pigmentation occurs even when nerve fragments are grafted into
tyrosinase null albino mice. Pigmentation defects are pervasive in
patients with neurofibromatosis type 1 (NF1). Mice hemizygous
for Nf1 mutations show enhanced pigmentation after nerve
lesion and occasionally form pigmented and unpigmented tumors. The
Nf1 nerve and the Nf1 host environment
both contribute to enhanced pigmentation. Grafted purified
Nf1 mutant glial cells [S100+-p75NGFR+-GFAP+-EGFR+
or
S100+-p75NGFR+-GFAP+-EGFR ]
mimic nerve-derived pigmentation. The NF1 protein, neurofibromin, is a
Ras-GAP that acts downstream of a few defined receptor tyrosine kinases, including [ -common (c)] the shared common
receptor for granulocyte and monocyte colony-stimulating factor,
interleukin-3 (IL3), and IL5. Cytokines in the environment have
the potential to suppress pigmentation as shown by nerve injury
experiments in null mice; when is c absent or
Nf1 is mutant, melanogenesis is increased. Thus, the adult nerve glial cell phenotype is maintained after nerve injury by
response to cytokines, through neurofibromin.
Key words:
Schwann cell; melanocyte; NF1; transdifferentiation; GMCSF; injury; stem cell
Copyright © 2002 Society for Neuroscience 0270-6474/02/22229831-10$05.00/0
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