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Updated: Sep 5, 2025

Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
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Muse cells decrease the neuroinflammatory response by modulating the proportion of M1 and M2 microglia in vitro.

Xin-Yao Yin1, Chen-Chun Wang1, Pan Du1

  • 1Department of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, China.

Neural Regeneration Research
|July 8, 2022
PubMed
Summary
This summary is machine-generated.

Multilineage-differentiating stress-enduring (Muse) cells reduce neuroinflammation by inhibiting key inflammatory pathways in microglia. These cells show promise for central nervous system (CNS) repair by modulating the inflammatory microenvironment.

Keywords:
bone marrow mesenchymal stem cellscentral nervous systemlipopolysaccharidemicrogliamultilineage-differentiating stress-enduring cellsneuroinflammationsignaling pathway

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Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Immunology

Background:

  • Neuroinflammation impedes central nervous system (CNS) repair after injury.
  • Stem cell transplantation is a potential therapeutic strategy for CNS disorders.
  • Identifying stem cells that promote nerve regeneration and improve the CNS microenvironment is challenging.

Purpose of the Study:

  • To investigate the anti-inflammatory effects and underlying mechanisms of multilineage-differentiating stress-enduring (Muse) cells.
  • To compare the efficacy of Muse cells against bone marrow mesenchymal stem cells in modulating neuroinflammation.

Main Methods:

  • Muse cells were isolated from bone marrow mesenchymal stem cells.
  • Muse cells were co-cultured with lipopolysaccharide-stimulated microglia in vitro.
  • Key inflammatory markers, microglial polarization (M1/M2), and signaling pathway proteins (TLR4/MyD88/NF-κB, p38 MAPK) were analyzed.

Main Results:

  • Muse cells significantly reduced pro-inflammatory cytokines (TNF-α, IL-1β) and increased anti-inflammatory cytokines (TGF-β, IL-10) in microglia.
  • Muse cells effectively shifted microglia from the M1 to the M2 phenotype.
  • Muse cells inhibited the TLR4/MyD88/NF-κB and p38 MAPK signaling pathways.

Conclusions:

  • Muse cells exhibit potent anti-neuroinflammatory effects by suppressing the TLR4/MyD88/NF-κB and p38 MAPK pathways in microglia.
  • Muse cells represent a promising cell source for CNS injury treatment due to their ability to mitigate neuroinflammation.
  • These findings provide valuable insights for selecting effective seed cells for CNS disease therapies.