Minocycline promotes remyelination in aggregating rat brain cell cultures after interferon-γ plus lipopolysaccharide-induced demyelination
Abstract
Minocycline has been shown to inhibit microglia reactivity, and to decrease the severity and progression of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. It remained to be examined whether minocycline was also able to promote remyelination. In the present study, myelinating aggregating brain cell cultures were used as a model to study the effects of minocycline on microglial reactivity, demyelination, and remyelination. Cultures were treated simultaneously with two inflammatory agents, interferon-γ (IFN-γ) and lipopolysaccharide (LPS), which caused an inflammatory response accompanied by demyelination. The inflammatory response was characterized by microglial reactivity, upregulation of inflammatory cytokines and iNOS, and increased phophorylation of P38 and P44/42 mitogen activated protein (MAP) kinases. Minocycline inhibited microglial reactivity, and attenuated the increased phophorylation of P38 and P44/42 MAP kinases. Demyelination, determined by a decrease in myelin basic protein (MBP) content and immunoreactivity 48 h after the treatment with the inflammatory agents, was not prevented by minocycline. However, 1 week after demyelination was assessed, the MBP content was restored in presence of minocycline, indicating that remyelination was promoted. Concomitantly, in cultures treated with minocycline, the markers of oligodendrocyte precursors cells (OPCs) and immature oligodendrocytes NG2 and O4, respectively, were decreased compared to cultures treated with the inflammatory agents only. These results suggest that minocycline attenuates microglial reactivity and favors remyelination by enhancing the differentiation of OPCs and immature oligodendrocytes.
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Inhibition of microglial activation by minocycline favors differentiation of oligodendrocyte precursors and immature oligodendrocytes, which are responsible for remyelination of neurons, an important event for improvement of MS condition.
“The inhibition of microglial activation by minocycline favors the differentiation of oligodendrocyte precursors and immature oligodendrocytes. These cells are responsible for remyelination of neurons, an important event for improvement of MS condition (Li et al., 2005; Yenari et al., 2006; Defaux et al., 2011; Miron et al., 2013).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Defaux et al., 2011
Minocycline is recognized as a microglia inhibitor.
“Minocycline has been recognized as a microglia inhibitor (Li et al., 2005; Defaux et al., 2011; Kobayashi et al., 2013; Miron et al., 2013; Huang et al., 2014).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Defaux et al., 2011
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References 53 · Cited by 40
- Authors
- Defaux, A., Zurich, M.-G., Honegger, P., & Monnet-Tschudi, F.
- Affiliations
- University of Lausanne (CH)
- ORCID
- Zurich, M.-G.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 187
- Pages
- 84-92
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2052197610
- Cited by
- 40
- References
- 53
- Citations by year
- 2023: 2 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 7 · 2013: 7 · 2012: 7
- FWCI
- 5.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- minocycline, remyelination, demyelination, microglial activation, interferon-gamma, lipopolysaccharide, oligodendrocyte precursor cells, myelin basic protein, MAPK phosphorylation, inducible nitric oxide synthase, neuroinflammation, multiple sclerosis
- MeSH terms
- Animals, Anti-Inflammatory Agents, Brain, Cell Differentiation, Cells, Cultured, Demyelinating Diseases, Enzyme Activation, Immunohistochemistry, Interferon-gamma, Lipopolysaccharides, Minocycline, Neurons, Oligodendroglia, Stem Cells, Blotting, Western, Signal Transduction, Reverse Transcriptase Polymerase Chain Reaction, Rats
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