TY - JOUR
T1 - Astrocyte-derived TGF-β2 and NGF differentially regulate neural recognition molecule expression by cultured astrocytes
AU - Saad, B.
AU - Constam, D. B.
AU - Ortmann, R.
AU - Moos, M.
AU - Fontana, A.
AU - Schachner, M.
PY - 1991
Y1 - 1991
N2 - Because of the importance of neural recognition molecules expressed by glial cells to mediate interactions with neurons, growth factors and cytokines known to be functional during morphogenesis and in diseases of the nervous system were studied for their effects on recognition molecule expression by cultured immature and mature astrocytes from several brain regions. In cultures of immature astrocytes, transforming growth factors-β1 (TGF-β1) and -β2 (TGF-β2) and nerve growth factor (NGF) increased expression of the neural adhesion molecule L1, leading to a glia-mediated L1-specific increase in neurite outgrowth of dorsal root ganglion neurons on the astrocyte substrate. L1 expression induced by TGF-β was inhibited by addition of antibodies to NGF, suggesting that TGF-β influences L1 expression by modulating production of NGF by astrocytes. TGF-β1 and -β2 decreased expression of N-CAM by immature astrocytes. Since N-CAM expression was not affected by NGF and antibodies to NGF did not abolish the TGF-β-induced decrease in N-CAM expression, NGF did not appear to be the mediator for regulating expression of N-CAM. Expression of the adhesion molecule on glia (AMOG) was not affected by any factor. NGF and TGF-β2 in latent form, but not TGF-β1 were found in the culture supernatants. Addition of interferon-γ (IFN-γ), interleukin-1β (IL-1β), interleukin-6 (IL-6), platelet-derived growth factor (PDGF), or basic fibroblast growth factor (bFGF) to the cultures did not change recognition molecule expression. Recognition molecule expression by mature astrocytes was not found to be modified by any of the factors tested. In view of the observation that levels of L1 and N-CAM expression correlated with the presence of TGF-β2 and NGF in the culture supernatants of immature astrocytes, an autocrine regulatory mechanism for recognition molecule expression by these cells is suggested to play a crucial role in regulation of neuron-glia interactions.
AB - Because of the importance of neural recognition molecules expressed by glial cells to mediate interactions with neurons, growth factors and cytokines known to be functional during morphogenesis and in diseases of the nervous system were studied for their effects on recognition molecule expression by cultured immature and mature astrocytes from several brain regions. In cultures of immature astrocytes, transforming growth factors-β1 (TGF-β1) and -β2 (TGF-β2) and nerve growth factor (NGF) increased expression of the neural adhesion molecule L1, leading to a glia-mediated L1-specific increase in neurite outgrowth of dorsal root ganglion neurons on the astrocyte substrate. L1 expression induced by TGF-β was inhibited by addition of antibodies to NGF, suggesting that TGF-β influences L1 expression by modulating production of NGF by astrocytes. TGF-β1 and -β2 decreased expression of N-CAM by immature astrocytes. Since N-CAM expression was not affected by NGF and antibodies to NGF did not abolish the TGF-β-induced decrease in N-CAM expression, NGF did not appear to be the mediator for regulating expression of N-CAM. Expression of the adhesion molecule on glia (AMOG) was not affected by any factor. NGF and TGF-β2 in latent form, but not TGF-β1 were found in the culture supernatants. Addition of interferon-γ (IFN-γ), interleukin-1β (IL-1β), interleukin-6 (IL-6), platelet-derived growth factor (PDGF), or basic fibroblast growth factor (bFGF) to the cultures did not change recognition molecule expression. Recognition molecule expression by mature astrocytes was not found to be modified by any of the factors tested. In view of the observation that levels of L1 and N-CAM expression correlated with the presence of TGF-β2 and NGF in the culture supernatants of immature astrocytes, an autocrine regulatory mechanism for recognition molecule expression by these cells is suggested to play a crucial role in regulation of neuron-glia interactions.
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U2 - https://doi.org/10.1083/jcb.115.2.473
DO - https://doi.org/10.1083/jcb.115.2.473
M3 - Article
C2 - 1717486
VL - 115
SP - 473
EP - 484
JO - The Journal of cell biology
JF - The Journal of cell biology
SN - 0021-9525
IS - 2
ER -