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Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility

Jelena Krstić1, Hristina Obradović1, Aleksandra Jauković1

  • 1Laboratory for Experimental Hematology and Stem Cells Institute for Medical Research, University of Belgrade, Dr Subotića 4, 11129 Belgrade, Serbia.

Biochimica Et Biophysica Acta
|November 30, 2014
PubMed

Insights

Interleukin-17 (IL-17) enhances mesenchymal stem cell (MSC) migration and tissue repair by increasing urokinase type plasminogen activator (uPA) expression. This cytokine promotes MSC movement and adhesion, crucial for inflammatory responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Regenerative Medicine

Background:

  • Mesenchymal stem cells (MSCs) are crucial for tissue regeneration due to their migratory capacity.
  • Interleukin-17 (IL-17), a pro-inflammatory cytokine, influences various cellular functions, but its effect on MSC migration is unclear.
  • Understanding IL-17's role in MSC behavior is vital for developing new therapeutic strategies.

Purpose of the Study:

  • To investigate the effect of IL-17 on the migration and transmigration of peripheral blood-derived MSCs (PB-MSCs).
  • To elucidate the molecular mechanisms underlying IL-17-mediated MSC migration.
  • To determine if IL-17 influences PB-MSC adhesion to endothelial cells and fibronectin.

Main Methods:

  • Utilized wound healing assays and collagen gel assays to assess PB-MSC migration.
  • Analyzed the expression of urokinase type plasminogen activator (uPA) and matrix metalloproteinases (MMPs).
  • Investigated IL-17's impact on PB-MSC adhesion to endothelial cells and fibronectin, and transendothelial migration.

Main Results:

  • IL-17 significantly increased PB-MSC migration and mobilization.
  • IL-17 upregulated uPA expression in a manner dependent on ERK1,2 MAPK signaling.
  • IL-17 enhanced PB-MSC adhesion to endothelial cells and fibronectin, promoting transendothelial migration.

Conclusions:

  • IL-17 acts as a chemotropic factor for PB-MSCs, enhancing their motility and uPA expression.
  • IL-17-induced uPA expression is a key mechanism driving increased PB-MSC migration and adhesion.
  • These findings suggest IL-17 plays a significant role in modulating MSC behavior during inflammation.
Keywords:
Interleukin-17MigrationPeripheral blood mesenchymal stem cellsTransendothelial migrationUrokinase type plasminogen activator

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