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Related Experiment Video

Updated: May 30, 2026

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
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AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

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Multipotent mesenchymal stromal cells increase tPA expression and concomitantly decrease PAI-1 expression in

Hongqi Xin1, Yi Li, Li Hong Shen

  • 1Department of Neurology, Henry Ford Hospital, Detroit, Michigan 48202, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|August 11, 2011
PubMed
Summary

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This summary is machine-generated.

Multipotent mesenchymal stromal cells (MSCs) boost brain repair by activating the sonic hedgehog (Shh) pathway in astrocytes. This process increases tissue plasminogen activator (tPA) and promotes neurite outgrowth after ischemic injury.

Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Molecular Biology

Background:

  • Multipotent mesenchymal stromal cells (MSCs) promote tissue repair.
  • MSCs enhance tissue plasminogen activator (tPA) activity in astrocytes at the ischemic boundary zone, stimulating neurite outgrowth.
  • The precise mechanisms of MSC-mediated tPA activation remain under investigation.

Purpose of the Study:

  • To investigate the role of the sonic hedgehog (Shh) signaling pathway in MSC-mediated tPA activation in astrocytes.
  • To elucidate the molecular mechanisms by which MSCs influence tPA and plasminogen activator inhibitor 1 (PAI-1) expression in astrocytes under ischemic conditions.

Main Methods:

  • In vitro models of ischemia using oxygen and glucose deprivation (OGD) and co-culture of astrocytes with MSCs.

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Last Updated: May 30, 2026

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  • Real-time PCR and Western blot analyses to quantify gene and protein expression levels.
  • Pharmacological inhibition of the Shh pathway using cyclopamine and genetic manipulation with Shh and Gli1 siRNA.

    • Main Results:

    • MSC co-culture significantly upregulated Shh levels in astrocytes, leading to increased tPA and decreased PAI-1 expression.
    • Inhibition of the Shh pathway with cyclopamine blocked MSC-induced changes in tPA and PAI-1.
    • Shh signaling modulated transforming growth factor-β1 (TGF-β1) levels, with MSCs and recombinant Shh decreasing TGF-β1, an effect reversed by cyclopamine.
    • Knockdown of Shh or Gli1 attenuated the effects of MSCs or recombinant Shh on tPA and PAI-1 expression.

    Conclusions:

    • MSCs activate the Shh signaling pathway in astrocytes following ischemic conditions.
    • The Shh pathway mediates the upregulation of tPA and downregulation of PAI-1 by MSCs, contributing to neuroprotection and repair.
    • These findings highlight the Shh pathway as a key mediator in MSC-based therapeutic strategies for ischemic brain injury.