Identification and partial purification of fibroblast growth factor from the brains of developing rats and leucodystrophic mutant mice

Logan, Ann; Berry, Martin; Thomas, GD; Gregson, N. A.; Logan, Susan

doi:10.1016/0306-4522(85)90266-0

Cited by 17 publications

(3 citation statements)

References 14 publications

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“…As discussed above, the failure of scarring in the cortex before the rat is 8 days old could be causally related to the failure of fibroblasts and macrophages to accumulate in the wound (see figure 14 a,b). Fibroblasts probably move into brain lesions in response to the elaboration of fibroblast tropic or trophic factors; one such molecule is fibroblast growth factor (FGF) which is found in high titres in neonatal and adult brains (Gospodarowicz 1988;Logan et al 1985). In the mature brain, elevated levels of FGF and of FGF mRNA are recorded during reactive gliosis and scarring (Finklestein et al 1988;Logan 1988;Nieto-Sampedro et al 1988).…”

Section: C) the Wound In The Cortex Of Animals Lesioned When Less Than 8 Days Oldmentioning

confidence: 99%

The response of the cerebral hemisphere of the rat to injury. II. The neonatal rat

Maxwell

Follows²,

Ashhurst

et al. 1990

Phil. Trans. R. Soc. Lond. B

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The response to injury of the cerebrum of the neonatal rat was studied in knife wounds by using both light and electron microscopical, and immunohistochemical, techniques. The rats were injured at 2, 4, 8, 12, 16 and 20 days post natum and the tissues examined 8 days later. A mature scar, that is, a layer of fibrous tissue separated from the injured neuropile by a glia limitans, is not formed in the brains of rats lesioned before 8 days post natum . Before this time, the neuropile of the severed hemisphere grows together and both the glia limitans externa and ventricular lining are repaired. The only evidence of the wound, 20 days after injury, is a subpial and periventricular accumulation of astrocytes and occasional groups of blood vessels; elsewhere glial and neuronal processes traverse the wound obliterating all signs of the original lesion. After 8 days post natum , scar tissue is deposited. The scar first appears in the superficial cortex as fibroblasts and macrophages invade from the meninges. With increasing age at injury, these cells penetrate more deeply and, after 16 days post natum at injury, the entire lesion contains these cells. Concomitantly, a glia limitans is formed over the walls of the lesion, firstly in the superficial cortex continuous with the glia limitans externa, and successively in the deeper cortex, white matter and corpus striatum as the meningeal fibroblasts and macrophages invade these regions. In the developing cerebrum, injured before 8 days post natum , the failure to form a scar is unrelated to the maturity of the astrocytes and fibroblasts, because both interact to regenerate the glia limitans externa. The development of a scar, in animals injured after 8 days post natum , is correlated with the failure of both axonal and dendritic regeneration. Because there are few oligodendrocytes, and no myelin, it appears that inhibition of axonal and dendritic growth is linked to scar formation, and not to putative inhibitory substrates such as those on the surface of oligodendrocytes, CNS scarring may be initiated by the invasion of fibroblasts and macrophages from the meninges into the injured neuropile. The possible reasons why these mesenchymal cells fail to penetrate before 8 days post natum are discussed.

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Section: C) the Wound In The Cortex Of Animals Lesioned When Less Than 8 Days Oldmentioning

confidence: 99%

The response of the cerebral hemisphere of the rat to injury. II. The neonatal rat

Maxwell

Follows²,

Ashhurst

et al. 1990

Phil. Trans. R. Soc. Lond. B

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“…NGF and bFGF are expressed in the nervous system in developing and adult organisms (Logan et al, 1985 ;Gospodarowicz et al ., 1986;Levi-Montalcini, 1987;Bothwell, 1991) . They play a critical role in the development of the sympathetic and sensory nervous systems, as well as an important role in the survival and development of neurons in the central nervous system (for reviews see, Thoenen and Barde, 1980;Wagner, 1991;Wagner and Kostyk, 1991;Gage et al, 1991).…”

mentioning

confidence: 99%

The activity of cAMP-dependent protein kinase is required at a posttranslational level for induction of voltage-dependent sodium channels by peptide growth factors in PC12 cells.

Ginty

Fanger

Wagner

et al. 1992

The Journal of Cell Biology

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. The synthesis and expression of voltagedependent sodium (Na) channels is a crucial aspect of neuronal differentiation because of the central role these ion channels play in the generation of action potentials and the transfer of information in the nervous system . We have used rat pheochromocytoma (PC12) cell lines deficient in cAMP-dependent protein kinase (PKA) activity to examine the role of PKA in the induction of Na channel expression by nerve growth factor (NGF) and basic FGF (bFGF) . In the parental PC12 cell line both NGF and bFGF elicit an increase in the density of functional Na channels, as determined from whole-cell patch clamp recordings. This increase does VOLTAGE-dependentsodium(Na)channelsp lay a central role in the production and propagation of action potentials in electrically excitable cells (Hodgkin and Huxley, 1952), and ultimately play a key role in the coding and transfer of information in the nervous system . This makes the synthesis of Na channels and acquisition of electrical excitability a crucial aspect of neuronal differentiation and suggests that an analysis of the mechanisms governing Na channel expression will reveal processes fundamental to the development of the nervous system. Na channels purified from mammalian brain contain a glycoprotein of ti 260 kD, termed the a subunit, as their principal component. Associated with the a subunit of the channels from mammalian brain are a ßl subunit of 36 kD and a 02 subunit of 33 kD (Hartshorne et al., 1982 ;Hartshorne and Catterall, 1984). Although the ß subunits may modify the functional properties ofNa channels, injection of Xenopus oocytes with mRNA encoding the a subunit alone is sufficient to produce functional Na channels (Noda et al.,

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“…N 'ERV~ growth factor (NGF), ~ acidic fibroblast growth factor (aFGF), and basic fibroblast growth factor (bFGF) promote survival and differentiation of specific classes of neuronal cells (5,13,21,27,32,38,40,41,43,45,46). NGF and the fibroblast growth factors (FGFs) are found in the peripheral and central nervous system in developing and adult organisms (14,26,28). The ability of each of these factors to act upon neuronal cells and their presence throughout the nervous system suggest that they may play a critical role in the development and/or maintenance of the nervous system.…”

mentioning

confidence: 99%

Nerve growth factor and fibroblast growth factor regulate neurite outgrowth and gene expression in PC12 cells via both protein kinase C- and cAMP-independent mechanisms.

Damon

D’Amore

Wagner

1990

The Journal of Cell Biology

120

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Abstract. Nerve growth factor (NGF), acidic fibroblast growth factor (aFGF), and basic fibroblast growth factor (bFGF) promote the survival and differentiation of a variety of peripheral and central neurons. The signal transduction mechanisms that mediate the actions of these factors in neuronal cells are not well understood. We examined the effect of a deficiency in protein kinase C (PKC) and/or cAMP second messenger systems on the actions of NGF, aFGF, and bFGF in the pheoehromocytoma (PC12) cell line. Activation of PKC was not required for NGF, aFGF, and bFGF to maximally induce ornithine decarboxylase (ODC), transcription of the early response genes, d2 and d5, or neurite outgrowth. In a PC12 cell mutant that is deficient in cAMP responsiveness (A126-1B2), all three growth factors maximally induced the transcription of d5 and neurite outgrowth, but aFGF and bFGF did not induce significant increases in ODC. NGF and aFGF maximally induced the transcription of d2 in A126-1B2 cells, but bFGF-induced d2 transcription was attenuated. NGF, aFGF, and bFGF maximally induced neurite outgrowth and d5 transcription in A126 cells that were made deficient in PKC. The d2 transcriptional response was substantially reduced in cells deficient in both PKC and cAMP responsiveness. These observations lead us to conclude that (a) cAMPand PKC-dependent events are, at least in part, causally linked to NGF, aFGF, and bFGF induction of both ODC and transcription of d2 and may control functionally redundant pathways; (b) NGF, aFGF, and bFGF can elicit neurite outgrowth and increase transcription of d2 and d5 in PC12 cells via mechanisms that are independent of both PKC and cAMP; (c) NGF, aFGF, and bFGF can induce ODC in the absence of PKC; and (d) aFGF and bFGF require cAMP responsiveness to induce ODC in PC12 cells.

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Identification and partial purification of fibroblast growth factor from the brains of developing rats and leucodystrophic mutant mice

Cited by 17 publications

References 14 publications

The response of the cerebral hemisphere of the rat to injury. II. The neonatal rat

The response of the cerebral hemisphere of the rat to injury. II. The neonatal rat

The activity of cAMP-dependent protein kinase is required at a posttranslational level for induction of voltage-dependent sodium channels by peptide growth factors in PC12 cells.

Nerve growth factor and fibroblast growth factor regulate neurite outgrowth and gene expression in PC12 cells via both protein kinase C- and cAMP-independent mechanisms.

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