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GM‐CSF promotes proliferation of human fetal and adult microglia in primary cultures
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 (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]
In the citing paper
“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]
In the citing paper
“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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Acevedo, G. (2013) · Rutgers University Community Repository (Rutgers University) · doi:10.7282/t3ks6q8v
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Metadata
- Authors
- Lee, S. C., Liu, W., Brosnan, C. F., & Dickson, D. W.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Lee, Sunhee C.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 1994-12
- Volume
- 12
- Issue
- 4
- Pages
- 309-318
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- 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
- 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 › Clinical Neurology › 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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