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Cited by 212Neuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanismsMultiple Sclerosis Research Studies

GM‐CSF promotes proliferation of human fetal and adult microglia in primary cultures

Lee, Sunhee C., Liu, Wei, Brosnan, Celia F., Dickson, Dennis W.·1994·Glia
DOI 10.1002/glia.440120407
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Abstract

Proliferation of microglia/macrophages is a common finding in many central nervous system diseases. To identify mitogenic signals for human microglia, we examined primary cultures of human fetal and adult microglia after stimulation with cytokines, colony stimulating factors (CSFs), or LPS, using proliferating cell nuclear antigen (PCNA) expression as an index of cell proliferation. The results showed that both M-CSF and GM-CSF induced microglial proliferation in fetal and adult human cultures, but that GM-CSF provided a much stronger stimulus. At 96 h post-stimulation, the mean PCNA labeling index was 2.4 for M-CSF and 13.3 for GM-CSF in fetal microglia; in adult microglia, the PCNA labeling index was 4.7 for M-CSF and 9.0 for GM-CSF. The effect of GM-CSF on fetal microglia was dose dependent and synergistic with M-CSF. LPS abolished the basal level of PCNA labeling in adult microglia, but in fetal microglia, caused a slight increase in PCNA labeling (1.9) at 96 h and consistently enhanced microglial cell survival and differentiation into highly branched cells. The production of GM-CSF in purified human fetal astrocyte and microglial cultures was examined after stimulation with LPS, TNF-alpha, or IL-1 beta. Unlike M-CSF, neither cell type produced GM-CSF in unstimulated cultures; however, when stimulated with IL-1 beta, astrocytes expressed GM-CSF mRNA and protein, which accumulated in the culture through 72 h. In microglia, LPS was the only effective inducing agent. An immu…

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  • CSF-1R is the main receptor for CSF-1.

    “CSF-1R is the main receptor for CSF-1 (also known as M-CSF), which is one of two major macrophage trophic factors, with CSF-2 (also known as GM-CSF) being the other [26].”

    From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [26]

  • CSF-2 promotes migration of blood-borne monocytes across the blood-brain barrier, which then differentiate into macrophages in the presence of CSF-1 and CSF-2.

    “CSF-2 promotes migration of blood-borne monocytes across the blood-brain barrier, which then differentiate into macrophages in the presence of CSF-1 and CSF-2 [16, 17, 26, 52].”

    From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [26]

  • The unique vulnerability of frontal white matter in HDLS may be accounted for by differences in abundance of the two main microglial trophic factors between brain regions, with CSF-2 being significantly up-regulated in gray matter compared to white matter and vice versa for CSF-1.

    “The unique vulnerability of frontal white matter in HDLS may also be accounted for by differences in abundance of the two main microglial trophic factors between brain regions, with CSF-2 being significantly up-regulated in gray matter compared to white matter and vice versa for CSF-1 [26].”

    From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [26]

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Authors
Lee, S. C., Liu, W., Brosnan, C. F., & Dickson, D. W.
Affiliations
Albert Einstein College of Medicine (US)
Corresponding author
Lee, Sunhee C.
ORCID
Venue
Glia
Publisher
Wiley
Published
1994-12
Volume
12
Issue
4
Pages
309-318
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
DOI
10.1002/glia.440120407
OpenAlex
W2089389165
Cited by
209
References
33
Citations by year
2025: 2 · 2024: 7 · 2023: 5 · 2022: 5 · 2021: 8 · 2020: 7 · 2019: 4 · 2018: 9 · 2017: 8 · 2016: 5 · 2015: 6 · 2014: 3 · 2013: 4 · 2012: 6
FWCI
5.59
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3603 d)
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p01mh047667-05)
  • National Institute on Aging (AG60803)
  • National Institute of Mental Health (MH 47667)
  • National Institute of Neurological Disorders and Stroke (NS-11920)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
Keywords
GM-CSF, macrophage colony-stimulating factor, microglial proliferation, colony-stimulating factors, LPS, proliferating cell nuclear antigen, IL-1β, multiple sclerosis, microglial activation, mitogenic signaling
MeSH terms
CD68 Molecule, Aged, Aged, 80 and over, Aging, Astrocytes, Cell Differentiation, Cell Division, Cell Survival, Cells, Cultured, Drug Synergism, Fetus, Humans, Lipopolysaccharides, Middle Aged, RNA, Messenger, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Macrophage Colony-Stimulating Factor, Granulocyte-Macrophage Colony-Stimulating Factor, Microglia, Proliferating Cell Nuclear Antigen

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