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Journal of Neuroscience, Vol 15, 419-428, Copyright © 1995 by Society for Neuroscience
Transforming growth factor-beta blocks myelination but not ensheathment of axons by Schwann cells in vitro
V Guenard, LA Gwynn and PM Wood
Miami Project to Cure Paralysis, University of Miami School of Medicine, Florida 33136.
Mechanisms regulating Schwann cell differentiation into a myelinating or a
mature nonmyelinating phenotype during development are poorly understood.
Humoral factors such as members of the transforming growth factor-beta
(TGF-beta) family, which are found in the developing and adult mammalian
nervous system and are known to affect cell differentiation, could be
involved. We tested the effects of TGF-beta isoforms on the ensheathment
and myelination of dorsal root ganglion (DRG) neurons by Schwann cells in
vitro. Rat embryonic DRG neurons and Schwann cells from the sciatic nerve
were isolated, purified, and recombined. In serum-free conditions, TGF-beta
blocked both Schwann cell myelination and the expression of the
myelin-related molecules galactocerebroside, P0, myelin-associated
glycoprotein, and myelin basic protein. In contrast, the expression of
molecules characteristic of mature nonmyelinating Schwann cells, including
neural-cell adhesion molecule, L1, and nerve growth factor receptor, was
maintained when compared to Schwann cells in nondifferentiated cultures.
Notably, the expression of glial fibrillary acidic protein, which is
expressed only in mature nonmyelinating Schwann cells in vivo, was
increased 10-fold in our cultures by TGF-beta. Electron microscopic
analysis indicated that in the presence of TGF-beta, basal lamina
deposition by Schwann cells was slightly increased. Most importantly, many
axons in TGF-beta- treated cultures received ensheathment typical of mature
nonmyelinated nerves. These effects of TGF-beta were partially reversed by
specific neutralizing anti-TGF-beta antibodies. We interpret these results
as evidence that TGF-beta regulates Schwann cell differentiation in vitro
by blocking the expression of the myelinating phenotype and promoting the
development of the nonmyelinating phenotype.
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