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Up-Regulated Expression of Matrix Metalloproteinases in Endothelial Cells Mediates Platelet Microvesicle-Induced

Cheng Sun1, Shi-Bin Feng1, Zheng-Wang Cao2

  • 1Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|May 3, 2017
PubMed
Abstract

Insights

Platelet microvesicles (PMVs) enhance blood vessel formation by increasing endothelial cell migration and tube formation. This process involves up-regulating matrix metalloproteinase (MMP) expression, independent of direct factor delivery.

Area of Science:

  • Cell Biology
  • Vascular Biology
  • Biochemistry

Background:

  • Platelet microvesicles (PMVs) are known to influence angiogenesis and vasculogenesis.
  • The precise mechanisms by which PMVs regulate endothelial cell (EC) function remain incompletely understood.
  • This study explores mechanisms beyond simple factor transport.

Purpose of the Study:

  • To investigate the role of PMVs in regulating EC angiogenic properties.
  • To determine if PMVs influence EC migration and network formation.
  • To elucidate the underlying molecular mechanisms, focusing on matrix metalloproteinases (MMPs).

Main Methods:

  • In vitro assays: Matrigel tube formation, transwell migration, and wound-healing assays using human umbilical vein endothelial cells (HUVECs).
  • Molecular analysis: Real-time PCR and western blot for pro-angiogenic factors.
  • Enzyme activity assays: Gelatin zymography for MMP-2 and MMP-9 activity.
  • In vivo validation: Matrigel plug assay in mice and testing of MMP inhibitors.

Main Results:

  • PMVs significantly promoted HUVEC capillary-like network formation and migration in a dose-dependent manner.
  • PMV treatment led to increased expression and activity of MMP-2 and MMP-9 in HUVECs.
  • Inhibition of MMPs attenuated the pro-angiogenic and pro-migratory effects of PMVs.
  • In vivo studies confirmed PMV-induced angiogenesis, which was reduced by MMP blockade.

Conclusions:

  • PMVs promote angiogenesis and endothelial cell migration through mechanisms involving the up-regulation of MMP expression.
  • This effect extends beyond the direct transfer of angiogenic factors from platelets.
  • MMPs play a crucial role in mediating the pro-angiogenic actions of PMVs.
Keywords:
AngiogenesisHuman umbilical vein endothelial cellMatrix metalloproteinasePlatelet microvesicle

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