Related Experiment Video

Updated: Aug 15, 2026

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
06:14

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Published on: June 11, 2017

Microparticles from apoptotic vascular smooth muscle cells induce endothelial dysfunction, a phenomenon prevented by

Sanah Essayagh1, Anne-Cecile Brisset, Anne-Dominique Terrisse

  • 1EA 2049, Laboratoire de Recherche sur la Thrombose, Université Paul Sabatier, Toulouse, France.

Thrombosis and Haemostasis
|November 8, 2005
PubMed

Insights

Apoptotic microparticles from smooth muscle cells impair blood vessel function by reducing nitric oxide release. Beta3-integrin antagonists may improve microvascular perfusion by blocking these effects.

Area of Science:

  • Cardiovascular Biology
  • Endothelial Function
  • Atherosclerosis Research

Background:

  • Fragile atherosclerotic plaques contain apoptotic smooth muscle cells (SMCs) and macrophages, which generate procoagulant microparticles (MPs).
  • These MPs can interact with the endothelium and potentially affect vascular reactivity.

Purpose of the Study:

  • To investigate the effects of apoptotic SMC-derived MPs on aortic vaso-reactivity and endothelial nitric oxide (NO) production.
  • To elucidate the underlying mechanisms and potential therapeutic targets.

Main Methods:

  • In vitro preparation of apoptotic MPs from SMCs.
  • Ex vivo mouse aorta ring preincubation and vaso-reactivity assessment.
  • In vitro studies using cultured endothelial cells to measure NO production.
  • Pharmacological inhibition using beta3-integrin antagonists (abciximab, eptifibatide) and enzymatic treatment (trypsin).

Main Results:

  • Apoptotic MPs dose-dependently reduced acetylcholine-induced vasodilation in aorta rings.
  • This effect was prevented by beta3-integrin antagonists, suggesting a role for this integrin.
  • MPs inhibited bradykinin-stimulated NO production in endothelial cells.
  • MP-induced endothelial dysfunction was redox-sensitive and abrogated by trypsin treatment, but independent of coagulation proteases.
  • Eptifibatide prevented the metabolic effects of MPs.

Conclusions:

  • Apoptotic SMC-derived MPs impair endothelial function by inhibiting NO production, mediated by beta3-integrin interactions.
  • This provides a potential platelet-independent mechanism explaining the therapeutic benefits of beta3-integrin antagonists in improving microvascular perfusion.

More Related Videos

Micropatterning and Assembly of 3D Microvessels13:05

Micropatterning and Assembly of 3D Microvessels

Published on: September 9, 2016

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption09:20

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Published on: October 4, 2019

Related Concept Videos

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...