Elsevier

Neuroscience Letters

Volume 73, Issue 3, 27 January 1987, Pages 287-292
Neuroscience Letters

Platelet-derived growth factor is a mitogen for glial but not for neuronal rat brain cells in vitro

https://doi.org/10.1016/0304-3940(87)90260-6Get rights and content

Abstract

The effects of platelet-derived growth factor (PDGF) on the proliferation of isolated rat neural cells grown in serum-free chemically defined media have been investigated. It was found that PDGF drastically stimulates the proliferation of astroblasts and oligodendroblasts, but has no effect on the proliferation of neuroblasts in primary culture. A role of PDGF in the reactive gliosis, occurring after brain injury, can be suggested.

References (30)

  • B. Pettmann et al.

    Purification of two astroglial growth factors from bovine brain

    FEBS Lett.

    (1985)
  • C.D. Scher et al.

    Platelet-derived growth factor and the regulation of the mammalian fibroblast cell cycle

    Biochim. Biophys. Acta

    (1979)
  • M. Weibel et al.

    Chemically defined medium for rat astroglial cells in primary culture

    Int. J. Dev. Neurosci.

    (1984)
  • B. Westermark et al.

    A platelet factor stimulating human normal glial cells

    Exp. Cell Res.

    (1976)
  • E.N. Benveniste et al.

    Stimulation of oligodendroglial proliferation and maturation by interleukin 2

    Nature (London)

    (1986)
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