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Platelet-derived microvesicles drive vascular smooth muscle cell migration via forming podosomes and promoting matrix

He Ren1, Jiahe Chen1, Kai Huang2

  • 1Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, Beijing, 100083, China.

Mechanobiology in Medicine
|May 21, 2025
PubMed

Insights

Platelet-derived microvesicles (PMVs) promote vascular smooth muscle cell (VSMC) migration by inducing podosome formation and matrix metalloproteinase-9 (MMP-9) activity, revealing a new mechanism in vascular intimal injury.

Area of Science:

  • Vascular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Platelet-derived microvesicles (PMVs) are implicated in vascular intimal injury, affecting vascular smooth muscle cell (VSMC) proliferation, migration, and metabolism.
  • The precise mechanisms by which PMVs induce VSMC migration remain incompletely understood.

Purpose of the Study:

  • To investigate the role of podosomes in mediating matrix metalloproteinase-9 (MMP-9) dependent VSMC migration induced by PMVs.
  • To elucidate a novel mechanism of PMV-induced VSMC migration.

Main Methods:

  • Isolation and identification of VSMCs from Sprague Dawley (SD) rat aortas.
  • Isolation and activation of platelets from SD rat blood.
  • Transwell co-culture system to assess PMV-induced VSMC migration.
  • Gene Ontology (GO) analysis to identify platelet proteins involved in podosome assembly.
  • Gelatin zymography and gelatin degradation assays to evaluate MMP-9 activity and extracellular matrix (ECM) remodeling.

Main Results:

  • Platelet proteins are involved in the positive regulation of podosome assembly, with many found in extracellular exosomes.
  • Activated platelets indirectly induced VSMC migration via releasing PMVs.
  • VSMCs formed podosomes, invasive protrusions that mediate ECM remodeling, leading to cell migration.
  • MMP-9 activity was robustly activated in VSMCs, facilitating podosome function and ECM degradation.
  • Gelatin degradation was observed in VSMCs co-cultured with platelets.

Conclusions:

  • PMVs promote VSMC migration through a novel mechanism involving podosome formation.
  • PMV-induced VSMC migration is dependent on the activation of MMP-9 activity.
  • This study reveals a new pathway by which PMVs contribute to vascular intimal injury via podosome and MMP-9 mediated VSMC migration.
Keywords:
Matrix metalloproteinase-9 (MMP-9)MigrationPlatelet-derived microvesicles (PMVs)PodosomeVascular smooth muscle cells (VSMCs)

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