Regulation of astrocyte proliferation by FGF-2 and heparan sulfate in vivo

Gómez-Pinilla, F; Vu, Loan; Cw, Cotman

doi:10.1523/jneurosci.15-03-02021.1995

Cited by 110 publications

(63 citation statements)

References 44 publications

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“…FGF-2 was directly injected into the tissues around the injury site, since heparan sulfate proteoglycans present on cell surfaces and/or the extracellular matrix are reported to activate, stabilize, and preserve FGF-2. 23. 24 This administration improved locomotor function, as expected; however, FGF-2-induced fibronectin-positive cells (FIFs) were suspected to be involved in the restoration, because the large cystic cavities around the lesion site were filled with these cells.…”

mentioning

confidence: 65%

FGF-2-Responsive and Spinal Cord-Resident Cells Improve Locomotor Function after Spinal Cord Injury

Kasai

Jikoh

Fukumitsu

et al. 2014

Journal of Neurotrauma

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The adult central nervous system has only a limited capacity for axonal regeneration. In this study, fibroblast growth factor-2 (FGF-2) was injected once into the spinal cord tissue around the injury site immediately after complete spinal cord transection in rats. This treatment markedly improved the locomotor function of the animals. Histological analysis demonstrated that tissue composed of FGF-2-induced fibronectin-positive cells (FIFs) had infiltrated the injury site and filled large cystic cavities, into which numerous axons with growth-associated protein-43 immunoreactivity penetrated. The FIFs could also be cultured from the intact spinal cord tissue, demonstrating that they were resident in the noninjured spinal cord. They had a spindle-shaped morphology and enhanced expression of mRNAs of N-cadherin and neurotrophic factors, suggesting the beneficial properties of the FIFs for axonal regeneration. Thus, these results argue for the continual use of autologous transplantation as a novel and promising cell therapy for the treatment of spinal cord injury.

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mentioning

confidence: 65%

FGF-2-Responsive and Spinal Cord-Resident Cells Improve Locomotor Function after Spinal Cord Injury

Kasai

Jikoh

Fukumitsu

et al. 2014

Journal of Neurotrauma

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“…Therefore, the next step was to determine whether any of the FGF family members could induce boundary formation between these cell types. FGF2 is the most likely candidate, because it is expressed in the brain after birth by neurons and astrocytes, it binds to FGFR1 (Gó mez-Pinilla et al, 1995), and it is upregulated after injury, contributing to glial scar formation (Eddleston and Mucke 1993;Goddard et al, 2002). FGF2 can also stimulate astrocyte proliferation, hypertrophy, changes in morphology, and an increase in GFAP expression (Eclancher et al, 1996;Goddard et al, 2002).…”

Section: Fgf Signalingmentioning

confidence: 99%

FGF/Heparin Differentially Regulates Schwann Cell and Olfactory Ensheathing Cell Interactions with Astrocytes: A Role in Astrocytosis

Santos-Silva¹,

Fairless²,

Frame³

et al. 2007

J. Neurosci.

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After injury, the CNS undergoes an astrocyte stress response characterized by reactive astrocytosis/proliferation, boundary formation, and increased glial fibrillary acidic protein (GFAP) and chondroitin sulfate proteoglycan (CSPG) expression. Previously, we showed that in vitro astrocytes exhibit this stress response when in contact with Schwann cells but not olfactory ensheathing cells (OECs). In this study, we confirm this finding in vivo by demonstrating that astrocytes mingle with OECs but not Schwann cells after injection into normal spinal cord. We show that Schwann cell-conditioned media (SCM) induces proliferation in monocultures of astrocytes and increases CSPG expression in a fibroblast growth factor receptor 1 (FGFR1)-independent manner. However, SCM added to OEC/astrocyte cocultures induces reactive astrocytosis and boundary formation, which, although sensitive to FGFR1 inhibition, was not induced by FGF2 alone. Addition of heparin to OEC/astrocyte cultures induces boundary formation, whereas heparinase or chlorate treatment of Schwann cell/astrocyte cultures reduces it, suggesting that heparan sulfate proteoglycans (HSPGs) are modulating this activity. In vivo, FGF2 and FGFR1 immunoreactivity was increased over grafted OECs and Schwann cells compared with the surrounding tissue, and HSPG immunoreactivity is increased over reactive astrocytes bordering the Schwann cell graft. These data suggest that components of the astrocyte stress response, including boundary formation, astrocyte hypertrophy, and GFAP expression, are mediated by an FGF family member, whereas proliferation and CSPG expression are not. Furthermore, after cell transplantation, HSPGs may be important for mediating the stress response in astrocytes via FGF2. Identification of factors secreted by Schwann cells that induce this negative response in astrocytes would further our ability to manipulate the inhibitory environment induced after injury to promote regeneration.

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“…bFGF has been shown to have a marked mitogenic effect on a wide range of tissues, including oligodendrocytes and astrocytes (Perraud et al, 1988;Vick and DeVries, 1992;Gomez-Pinilla et al, 1995), and to stimulate the secretion of other growth factors by glial cells (Yoshida and Gage, 1991). A large increase in numbers of glial cells has not been observed in the cut optic nerve stumps (R.E.…”

Section: Bfgf Increases Survival Of Ganglion Cellsmentioning

confidence: 99%

Basic fibroblast growth factor applied to the optic nerve after injury increases long-term cell survival in the frog retina

et al. 2000

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The neuroprotective effects of basic fibroblast growth factor (bFGF) on the long-term survival of axotomized retinal ganglion cells (RGCs) were studied in the frog Rana pipiens. Cell loss was quantified in different regions of the ganglion cell layer using Nissl staining and tetramethylrhodamine dextran amine backfilling. All regions of the retina showed a significant decrease (32-66%) in RGC numbers between 4 and 16 weeks after axotomy. Some cells showed morphological and biochemical signs of apoptosis. A single application of bFGF to the optic nerve stump at the time of axotomy protected many of the cells 6 weeks after the injury, but this effect was lost by 12 weeks. A second application of bFGF, 6 weeks after the injury, rescued many RGCs at 12 weeks. In contrast, single or double injections of bFGF into the eyeball had no effect on RGC survival. Axotomized RGCs were significantly enlarged and elongated after axotomy, and these morphological changes were increased by bFGF treatment. In the normal retina and optic nerve, immunocytochemical staining showed bFGF-like immunoreactivity (-LI) in the pigment epithelial layer, in the outer segments of photoreceptors, and in occasional RGCs. Strong bFGF-LI was present in Müller cells and in optic nerve astrocytes and oligodendrocytes. FGF receptor-LI was present in photoreceptors, outer plexiform layer, retinal ganglion cell axons, and Müller cells. FGF receptor-LI was also observed in optic nerve glia.

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Regulation of astrocyte proliferation by FGF-2 and heparan sulfate in vivo

Cited by 110 publications

References 44 publications

FGF-2-Responsive and Spinal Cord-Resident Cells Improve Locomotor Function after Spinal Cord Injury

FGF-2-Responsive and Spinal Cord-Resident Cells Improve Locomotor Function after Spinal Cord Injury

FGF/Heparin Differentially Regulates Schwann Cell and Olfactory Ensheathing Cell Interactions with Astrocytes: A Role in Astrocytosis

Basic fibroblast growth factor applied to the optic nerve after injury increases long-term cell survival in the frog retina

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