Cited by 81Nerve injury and regenerationNeurogenesis and neuroplasticity mechanismsAxon Guidance and Neuronal Signaling

Platelet-derived growth factor is constitutively secreted from neuronal cell bodies but not from axons

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Fruttiger, Marcus, Calver, Andrew R., Richardson, William D.·2000·Current Biology

Abstract

Neurons synthesise and secrete many growth and survival factors but it is not usually clear whether they are released locally at the cell body or further afield from axons or axon terminals. Without this information, we cannot predict the site(s) of action or the biological functions of many neuron-derived factors. For example, can neuronal platelet-derived growth factor (PDGF) be secreted from axons and reach glial cells in nerve-fibre (white-matter) tracts? To address this question, we expressed PDGF-A in retinal ganglion neurons in transgenic mice and tested for release of PDGF from cell bodies in the retina and from axons in the optic nerve. In both the retina and optic nerve, there are glial cells that express PDGF receptor alpha (PDGFR alpha) [1] and divide in response to PDGF [2-5], so we could detect functional PDGF indirectly through the mitogenic response of glia at both locations. Expressing PDGF-A in neurons under the control of the neuron-specific enolase promoter (NSE-PDGF-A) resulted in a striking hyperplasia of retinal astrocytes, demonstrating that PDGF is secreted from the cell bodies of neurons in the retina [4]. In contrast, glial proliferation in the optic nerve was unaffected, indicating that PDGF is not released from axons. When PDGF was expressed directly in the optic nerve under the control of an astrocyte-specific promoter (GFAP-PDGF-A), oligodendrocyte progenitors hyperproliferated, resulting in a hypertrophic optic nerve. We conclude that PDGF is constitutively secreted from neuronal cell bodies in vivo, but not from axons in white-matter tracts.

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Crossref · 10.1016/s0960-9822(00)00757-0

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  • Pdgf-AA is released from neuronal cell bodies in the retina but not from their axons in the optic nerve.

    “Against this idea, we showed previously that an important neuron-derived OP mitogen, platelet-derived growth factor (A-chain homodimers, Pdgf-AA), is released from neuronal cell bodies in the retina but not from their axons in the optic nerve (Fruttiger et al., 2000).”

    From Oligodendrocyte Dynamics in the Healthy Adult CNS: Evidence for Myelin Remodeling (2013) · cites this paper as Fruttiger et al., 2000

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Authors
Fruttiger, M., Calver, A. R., & Richardson, W. D.
Affiliations
  • University College London (GB)
  • GlaxoSmithKline (United Kingdom) (GB)
Corresponding author
Fruttiger, Marcus
Venue
Current Biology
Publisher
Elsevier BV
Published
2000-10
Volume
10
Issue
20
Pages
1283-1286
ISSN
0960-9822 (ISSN-L)
OpenAlex
W2125294887
Cited by
81
References
19
Citations by year
2026: 2 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 8 · 2014: 3 · 2013: 7 · 2012: 5
FWCI
1.16
Type
journal article
Language
en
Open access
Locations
  • Current Biology (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
Keywords
platelet-derived growth factor, PDGF-A, neuronal cell bodies, axons, axon terminals, retinal ganglion cells, optic nerve, retinal astrocytes, oligodendrocyte progenitors, glial cell proliferation, PDGFRA, neuron-specific enolase promoter, GFAP promoter, white matter tracts, transgenic mice
MeSH terms
Animals, Astrocytes, Axons, Cell Division, Humans, Hyperplasia, Mice, Transgenic, Neuroglia, Neurons, Oligodendroglia, Optic Nerve, Phosphopyruvate Hydratase, Platelet-Derived Growth Factor, Promoter Regions, Genetic, Retina, Mice, Knockout, Mice

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