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Mesenchymal stem cells regulate angiogenesis according to their mechanical environment.

Grit Kasper1, Niels Dankert, Jens Tuischer

  • 1Musculoskeletal Research Center Berlin, Charité-Universitätsmedizin Berlin, Augustenburger Platz, 113353 Berlin, Germany. Grit.Kasper@charite.de

Stem Cells (Dayton, Ohio)
|January 16, 2007
PubMed
Summary

Mechanical loading enhances mesenchymal stem cells' (MSCs) ability to promote angiogenesis, crucial for bone healing. This paracrine effect involves fibroblast growth factor receptor 1 (FGFR1) and vascular endothelial growth factor receptor (VEGFR) signaling pathways.

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Published on: September 18, 2019

Area of Science:

  • Biomedical Engineering
  • Regenerative Medicine
  • Cell Biology

Background:

  • Mesenchymal stem cells (MSCs) are key drivers of fracture and bone defect healing.
  • MSCs promote angiogenesis, a critical process for tissue regeneration.
  • The influence of mechanical loading on MSCs' proangiogenic capacity requires further investigation.

Purpose of the Study:

  • To investigate the effect of mechanical loading on MSCs' proangiogenic potential.
  • To elucidate the molecular mechanisms underlying mechanically induced angiogenesis by MSCs.

Main Methods:

  • MSCs were subjected to mechanical stimulation.
  • Conditioned media from stimulated and unstimulated MSCs were used in 2D tube formation and 3D spheroid sprouting assays.
  • Endothelial cell proliferation, migration, and adhesion were assessed.
  • FGFR1 and VEGFR signaling pathways were analyzed.
  • Expression levels of angiogenic regulators were screened.

Main Results:

  • Conditioned media from mechanically stimulated MSCs significantly enhanced angiogenesis compared to unstimulated MSCs.
  • Mechanical stimulation primarily increased endothelial cell proliferation, not migration or adhesion.
  • Angiogenesis promotion was dependent on FGFR1 signaling and inhibited by VEGFR tyrosine kinase blocking.
  • Enrichment of MMP-2, TGF-β1, and bFGF, but not VEGF, was observed in response to mechanical stimulation.

Conclusions:

  • Mechanical loading of MSCs enhances their paracrine stimulation of angiogenesis.
  • The mechanism involves a network of angiogenic molecules and depends on FGFR and VEGFR signaling cascades.
  • This suggests a potential therapeutic strategy for bone regeneration by optimizing mechanical stimuli for MSCs.