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Updated: Sep 20, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
08:28

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Shedding of active tissue factor by aortic smooth muscle cells (SMCs) undergoing apoptosis

Anne-Cécile Brisset1, Anne-Dominique Terrisse, Dominique Dupouy

  • 1Laboratoire d'Hématologie, Pavillon Caubet, Hôpital Purpan, 31059 Toulouse Cedex, France.

Thrombosis and Haemostasis
|September 6, 2003
PubMed

Insights

Apoptosis of synthetic smooth muscle cells (SMCs) in atherosclerotic plaques increases their procoagulant potential. Shed microparticles from dying SMCs promote thrombus formation, highlighting thrombotic risks in advanced atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Thrombosis Research
  • Atherosclerosis Pathogenesis

Background:

  • Apoptosis of neo-intimal smooth muscle cells (SMCs) is characteristic of advanced atherosclerotic plaques.
  • SMCs in synthetic phenotype up-regulate Tissue Factor (TF) and Tissue Factor Inhibitor (TFPI), releasing significant TFPI.

Purpose of the Study:

  • To investigate the procoagulant properties of synthetic SMCs during apoptosis.
  • To determine the role of SMC-derived microparticles in thrombosis.

Main Methods:

  • Isolation of SMCs from rat aorta post-balloon injury.
  • Induction of apoptosis using Fas-ligand.
  • Measurement of surface TF activity, prothrombinase, and TFPI release.
  • Analysis of microparticle (MP) procoagulant function in vitro and in whole blood flow models.

Main Results:

  • Fas-ligand induced apoptosis in SMCs.
  • Surface TF activity increased 10-fold, with a proportional rise in prothrombinase, while membrane TF protein decreased.
  • Microparticles shed during SMC death carried functional TF, with unchanged TFPI release, shifting the balance towards a procoagulant state.
  • Shed MPs enhanced thrombus formation in flowing whole blood.

Conclusions:

  • Apoptotic SMCs in atherosclerotic plaques are a source of highly thrombogenic material.
  • Release of TF-bearing MPs during SMC death contributes to plaque thrombogenicity.
  • Plaque disruption can release this procoagulant material into circulation, increasing thrombotic risk.

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