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Journal of Neuroscience, Vol 11, 3165-3177, Copyright © 1991 by Society for Neuroscience
Cell-type-specific regulation of nerve growth factor (NGF) synthesis in non-neuronal cells: comparison of Schwann cells with other cell types
I Matsuoka, M Meyer and H Thoenen
Department of Neurochemistry, Max Planck Institute for Psychiatry, Planegg-Martinsried, Germany.
We have previously shown that after peripheral nerve lesion the synthesis
of NGF is induced in cells of the nerve sheath (Heumann et al., 1987a).
Further analysis led to the identification of growth factors and
intracellular mechanisms responsible for this induction in sciatic
fibroblasts (Lindholm et al., 1988; Hengerer et al., 1990). The present
work aimed at the elucidation of the regulation of NGF synthesis in Schwann
cells. A variety of cytokines and peptide growth factors, including
interleukin-1 (IL-1) and platelet-derived growth factor (PDGF), which are
known to increase NGF-mRNA in fibroblasts and astrocytes, failed to do so
in Schwann cell cultures. Forskolin (FK), an activator of adenylate
cyclase, increased the level of NGF-mRNA eightfold within 3 hr of
incubation. The effect of FK on NGF-mRNA was mimicked by analogs of cAMP
but not by dideoxyforskolin, an FK derivative not activating adenylate
cyclase. Application of norepinephrine and isoproterenol also augmented the
NGF-mRNA content. Pretreatment of Schwann cells with
N-[2-(methylamino)ethyl]-5- isoquinoline sulfonamide dihydrochloride (H-8),
an inhibitor of cyclic- nucleotide-dependent protein kinases, decreased
both basal and elevated levels of NGF-mRNA. Ionomycin, a Ca2+ ionophore,
and phorbol 12- myristate 13-acetate (TPA), an activator of protein kinase
C, potentiated the effect of FK in an H-8-sensitive manner. We show that
the action of FK is independent of changes in mRNA stability and of protein
synthesis. Thus, in cultured Schwann cells upregulation of NGF- mRNA
expression seems to be mainly achieved by a cAMP-triggered transcriptional
activation of the NGF gene. Another striking difference between various
glial cell types was revealed by application of transforming growth factor
beta-1 (TGF-beta 1), which is the strongest inducer of NGF-mRNA in cultured
astrocytes (Lindholm et al., 1990). Schwann cells responded to TGF-beta 1
by decreasing basal as well as FK- induced NGF-mRNA levels. Together with
previously published work, our results show that cell-type-specific
mechanisms not only account for the different control of NGF expression in
neurons as compared to glial cells, but also reveal a surprising
specificity of regulatory mechanisms in different non-neuronal cell types,
even those derived from the same tissue such as fibroblasts and Schwann
cells of peripheral nerves.
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