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Related Concept Videos

Mesenchymal Stem Cells01:19

Mesenchymal Stem Cells

Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their access...

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Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
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Multipotent mesenchymal stromal cells decrease transforming growth factor β1 expression in microglia/macrophages and

Hongqi Xin1, Michael Chopp, Li Hong Shen

  • 1Department of Neurology, Henry Ford Health System, Detroit, MI 48202, United States.

Neuroscience Letters
|March 19, 2013
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Multipotent mesenchymal stromal cells (MSCs) reduce transforming growth factor β1 (TGFβ1) in brain cells after stroke. This reduces plasminogen activator inhibitor 1 (PAI-1) levels, offering a potential therapeutic strategy.

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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury

Published on: September 4, 2013

Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Multipotent mesenchymal stromal cells (MSCs) modulate the brain's response to injury.
  • Transforming growth factor β1 (TGFβ1) plays a role in post-stroke inflammation and tissue remodeling.
  • Plasminogen activator inhibitor 1 (PAI-1) is implicated in glial activation and matrix deposition after stroke.

Purpose of the Study:

  • To investigate the effect of MSCs on TGFβ1 and PAI-1 expression in astrocytes and microglia/macrophages following ischemic stroke.
  • To determine the cellular sources and mechanisms by which MSCs influence TGFβ1 and PAI-1 pathways in the ischemic brain.

Main Methods:

  • In vivo studies using middle cerebral artery occlusion (MCAo) model in mice treated with MSCs.
  • In vitro studies utilizing astrocyte-microglia/macrophage co-cultures subjected to oxygen-glucose deprivation (OGD).
  • Analysis of TGFβ1, phosphorylated SMAD 2/3 (p-SMAD 2/3), and PAI-1 expression using RT-PCR and Western blot.

Main Results:

  • MSC treatment significantly decreased TGFβ1 protein in both astrocytes and microglia/macrophages in vivo.
  • MSCs reduced TGFβ1 mRNA in co-cultures under OGD conditions.
  • MSC administration significantly decreased PAI-1 mRNA and protein levels in astrocytes in vitro.
  • p-SMAD 2/3 was decreased in astrocytes after MSC treatment both in vivo and in vitro.

Conclusions:

  • MSCs effectively reduce TGFβ1 expression in both astrocytes and microglia/macrophages post-stroke.
  • The reduction in TGFβ1 by MSCs contributes to the downregulation of PAI-1 in astrocytes.
  • These findings highlight a novel mechanism for MSC-mediated neuroprotection involving the TGFβ1/PAI-1 axis.