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Valéry Combes1, Sharissa L Latham2, Beryl Wen2

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Diannexin, a homodimer of annexin V, inhibits microparticle release from endothelial cells by binding to phosphatidylserine (PS). This suggests a therapeutic potential for Diannexin in modulating microparticle-mediated processes in immunopathology.

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DiannexinMicroparticlesTNFcytokinesendotheliuminflammationvesiculation

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Area of Science:

  • Cell Biology
  • Immunology
  • Biochemistry

Background:

  • Microparticles are biological effectors involved in immunopathology.
  • Diannexin, an annexin V homodimer, binds phosphatidylserine (PS) with high affinity and inhibits coagulation.
  • The study investigates Diannexin's effect on microparticle production by endothelial cells.

Purpose of the Study:

  • To determine if Diannexin can modulate microparticle production by endothelial cells.
  • To investigate Diannexin's interaction with phosphatidylserine exposure during microparticle release.

Main Methods:

  • Utilized fluorescently labelled Diannexin to study binding to endothelial cells.
  • Assessed microparticle (MP) release from TNF-activated endothelial cells treated with Diannexin.
  • Employed scanning electron microscopy to analyze cell surface morphology.

Main Results:

  • Diannexin binds to activated endothelial cells and is incorporated into released microparticles.
  • Diannexin inhibits microparticle release from activated endothelial cells without preventing endothelial activation.
  • Observed morphological differences in cell surface protuberances following Diannexin treatment.

Conclusions:

  • Diannexin inhibits endothelial vesiculation by binding to phosphatidylserine (PS).
  • Diannexin's interaction occurs with PS on the cell surface and inner plasma membrane leaflet.
  • These findings suggest Diannexin's potential role in managing microparticle-related conditions.