Effects of acidic and basic fibroblast growth factors (aFGF and bFGF) on the proliferation and the glutamine synthetase expression of rat astroblasts in culture

Perraud, Frédéric; Besnard, François; Pettmann, Brigitte; Sensenbrenner, M.; Labourdette, G.

doi:10.1002/glia.440010204

Cited by 101 publications

(59 citation statements)

References 44 publications

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“…These results corroborate some of our previous results on astroblast proliferation and maturation obtained in various conditions [21,28]. Although the analyses of the autoradiograms have been done visually, the main result which is a similarity between the effects of aFGF and bFGF cannot be disputed since, with the same technical approach, in a previous work we have shown that epidermal growth factor and thrombin modulated the synthesis of many proteins differently than aFGF [20].…”

Section: Discussionsupporting

confidence: 90%

Acidic and basic fibroblast growth factors similarly regulate the rate of biosynthesis of rat astroblast proteins

Loret¹,

Laeng²,

Sensenbrenner³

et al. 1989

FEBS Letters

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Quiescent rat astroblasts in culture have been treated for various periods of time with acidic and basic fibroblast growth factors. Both factors elicited similar effects on the cell proliferation and glutamine synthetase activity. The rate of biosynthesis of the proteins analyzed on autoradiograms of polyacrylamide gels after two-dimensional electrophoresis was also similarly modulated by the two growth factors. These results suggest that the two fibroblast growth factors act through the same membrane receptors on rat astroblasts in culture.

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Section: Discussionsupporting

confidence: 90%

Acidic and basic fibroblast growth factors similarly regulate the rate of biosynthesis of rat astroblast proteins

Loret¹,

Laeng²,

Sensenbrenner³

et al. 1989

FEBS Letters

Self Cite

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“…Some of these effects with bFGF have been reported previously (Perraud et al, 1988). Effects of bFGF were evident after 24 h and were complete within 48 h, affecting all GFAP ϩ cells in the culture, as seen in Figure 1B.…”

Section: Effects Of Bfgf On Morphology Of Ca1/ca3 Hippocampal Astrocytessupporting

confidence: 78%

“…We have identified basic fibroblast growth factor (bFGF) as a potent inducer of process growth and membrane retraction in cultured astrocytes (see also Perraud et al, 1988). By expressing dominant inhibitory or constitutively active forms of the Ras family members, we have defined a signal transduction cascade in which bFGF, acting via Ha-Ras, inhibits Rac1 and RhoA.…”

Section: Introductionmentioning

confidence: 99%

Ras Family GTPases Control Growth of Astrocyte Processes

Kalman¹,

Gomperts

Hardy

et al. 1999

MBoC

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Astrocytes in neuron-free cultures typically lack processes, although they are highly process-bearing in vivo. We show that basic fibroblast growth factor (bFGF) induces cultured astrocytes to grow processes and that Ras family GTPases mediate these morphological changes. Activated alleles of rac1 and rhoA blocked and reversed bFGF effects when introduced into astrocytes in dissociated culture and in brain slices using recombinant adenoviruses. By contrast, dominant negative (DN) alleles of both GTPases mimicked bFGF effects. A DN allele of Ha-ras blocked bFGF effects but not those of Rac1-DN or RhoA-DN. Our results show that bFGF acting through c-Ha-Ras inhibits endogenous Rac1 and RhoA GTPases thereby triggering astrocyte process growth, and they provide evidence for the regulation of this cascade in vivo by a yet undetermined neuron-derived factor.

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“…7), again showing differential signal transduction for the apoE/HDL release by a P13K/Akt pathway and lipid biosynthesis by an MEK/ ERK pathway. DISCUSSION FGF-1 is a stimulant for proliferation and cell differentiation of mesodermal and neuroectodermal cells such as fibroblasts and astrocytes (35). Most studies of this factor have focused on its activity in promoting cell growth and differentiation.…”

Section: Fgf-1 Regulation Of Biogenesis Of Apoe-hdl In Astrocytesmentioning

confidence: 99%

Mechanism for FGF-1 to regulate biogenesis of apoE-HDL in astrocytes

Ito

Nagayasu

Okumura-Noji

et al. 2007

Journal of Lipid Research

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Fibroblast growth factor-1 (FGF-1) is secreted by astrocytes and stimulates apolipoprotein E (apoE)-HDL biogenesis by an autocrine mechanism to help in recovery from brain injury. In apoE-deficient mouse astrocytes, FGF-1 stimulated cholesterol biosynthesis without enhancing its release, indicating a signaling pathway independent of apoE biosynthesis upregulation. SU5402, an inhibitor of FGF receptor, inhibited FGF-1-induced phosphorylation of MEK, ERK, and Akt, as well as all the apoE-HDL biogenesis-related events in rat astrocytes. LY294002, an inhibitor of phosphatidylinositide 3-OH kinase (PI3K) and of Akt phosphorylation, inhibited apoE-HDL secretion but not cholesterol biosynthesis, whereas U0126, an inhibitor of MEK and of ERK phosphorylation, inhibited cholesterol biosynthesis but not apoE-HDL secretion. Increase of apoE-mRNA by FGF-1 was not influenced by either inhibitor. When rat apoE/pcDNA3. his was transfected to transformed rat astrocyte GA-1 cells that otherwise do not synthesize apoE (GA-1/25), FGF-1 did not influence apoE-mRNA, but did increase the apoE secretion and Akt phosphorylation that were suppressed by LY294002. Lipid biosynthesis was increased by FGF-1 in GA-1/25 cells and suppressed by U0126. FGF-1 upregulates apoE-HDL biogenesis by three independent signaling pathways. The PI3K/Akt pathway upregulates secretion of apoE/apoE-HDL, the MEK/ERK pathway stimulates cholesterol biosynthesis, and an unknown pathway enhances apoE transcription.-Ito, J-i., Y. Nagayasu, K. Okumura-Noji, R. Lu, T. Nishida, Y. Miura, K. Asai, A. Kheirollah, S. Nakaya, and S. Yokoyama. Mechanism for FGF-1 to regulate biogenesis of apoE-HDL in astrocytes. J. Lipid Res. 2007Res. . 48: 2020Res. -2027. Supplementary key words astrocytesNeuronal cells in the central nervous system (CNS), such as neurons, oligodendroglias, and astrocytes, all appear in unique shapes, with large cell surfaces, and accordingly contain large amounts of cholesterol. Cholesterol content in the CNS could thus account for 25-30% of total body cholesterol in humans (1, 2). Cholesterol plays many key roles in the CNS, including roles in neurite outgrowth (3, 4) and synapse formation (5).Cholesterol homeostasis in animals is maintained by intra-and extracellular regulation of its metabolism (6), and extracellular transport of cholesterol in vertebrates is carried by the plasma lipoprotein system. However, the blood-brain barrier prevents the CNS from accessing this system, so the CNS operates as a unique and independent CNS-specific lipoprotein system for extracellular cholesterol transport. HDL is a lipoprotein found exclusively in cerebrospinal fluid that contains mainly apolipoprotein E (apoE) and apoA-I (7). Although apoA-I is not synthesized by neural cells, and its origin is uncertain (8, 9), apoE is known to be synthesized, at least in astrocytes and microglias, to generate apoE-HDL (10, 11). Many reports suggest that apoE-HDL is a key lipoprotein in the delivery of cholesterol to the neural cells, and this lipoprotein seems to ...

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Effects of acidic and basic fibroblast growth factors (aFGF and bFGF) on the proliferation and the glutamine synthetase expression of rat astroblasts in culture

Cited by 101 publications

References 44 publications

Acidic and basic fibroblast growth factors similarly regulate the rate of biosynthesis of rat astroblast proteins

Acidic and basic fibroblast growth factors similarly regulate the rate of biosynthesis of rat astroblast proteins

Ras Family GTPases Control Growth of Astrocyte Processes

Mechanism for FGF-1 to regulate biogenesis of apoE-HDL in astrocytes

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