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Updated: Jun 2, 2026
Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
Effects of microglia-derived cytokines on astrocyte proliferation
A Suzumura1, M Sawada, K Mokuno
1Department of Neurology, School of Medicine, Fujita Health University, Toyoake, Aichi 470-11 (Japan).
Abstract:
Recent studies have suggested that cytokines, such as interleukin-l(IL-l), tumor necrosis factor(TNF)α, or interferon(IFN) γ, play a role in the development of astrocytic gliosis. In this study, we examined the effects of these cytokines on the proliferation of purified astrocytes in vitro, using the colorimetric assay, bromodeoxyuridine uptake by astrocytes, and changes in the amount of the S-100 β protein as markers of astrocyte proliferation. The effects of a crude supernatant from microglia enriched cultures (Mi-Sup) also were examined. In contrast to previous reports, these recombinant cytokines did not induce proliferation of purified mouse astrocytes. However, stimulation of astrocytes with Mi-Sup increased all the markers for astrocyte proliferation, which could not be blocked by the addition of anti-IL-1, IL-6, IFNγ or TGFβ antibodies. Thus, it appears that microglia produce factors, other than the above cytokines, which induce the proliferation of astrocytes in vitro. These factors may have a role in the development of gliosis in various pathologic conditions of the central nervous system.
Insights
Microglia-derived factors, not common cytokines, stimulate astrocyte proliferation in vitro. These findings suggest novel mechanisms underlying astrocytic gliosis in central nervous system diseases.
Area of Science:
- Neuroscience
- Immunology
Background:
- Astrocytic gliosis is implicated in CNS pathology.
- Cytokines like IL-1, TNFα, and IFNγ have been suggested to influence gliosis.
Purpose of the Study:
- To investigate the direct effects of specific cytokines on astrocyte proliferation.
- To determine if microglia-derived factors stimulate astrocyte proliferation.
Main Methods:
- Primary astrocyte cultures were used.
- Astrocyte proliferation was assessed using bromodeoxyuridine uptake and S-100β protein levels.
- Recombinant cytokines and microglia-supernatant (Mi-Sup) were applied.
Main Results:
- Recombinant interleukin-1 (IL-1), tumor necrosis factor-alpha (TNFα), and interferon-gamma (IFNγ) did not induce astrocyte proliferation.
- Microglia-supernatant significantly increased astrocyte proliferation markers.
- Antibodies against IL-1, IL-6, IFNγ, and TGFβ did not inhibit Mi-Sup-induced proliferation.
Conclusions:
- Cytokines commonly studied do not directly drive astrocyte proliferation in this model.
- Microglia produce uncharacterized factors that promote astrocyte proliferation in vitro.
- These novel microglial factors may play a significant role in astrogliosis during CNS disease.
