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On-Chip Endothelial Inflammatory Phenotyping
12:43

On-Chip Endothelial Inflammatory Phenotyping

Published on: July 21, 2012

Upregulation of proinflammatory proteins through NF-kappaB pathway by shed membrane microparticles results in

Angela Tesse1, M Carmen Martínez, Bénédicte Hugel

  • 1Pharmacologie et Physico-Chimie des Interactions Cellulaires et Moléculaires, UMR CNRS 7034, Illkirch, France.

Arteriosclerosis, Thrombosis, and Vascular Biology
|October 8, 2005
PubMed
Abstract

Insights

Microparticles from T cells or diabetic patients cause vascular hyporeactivity. This effect, linked to inflammation, is reversed by inhibiting nitric oxide (NO) and cyclooxygenase-2 pathways.

Area of Science:

  • Vascular Biology
  • Immunology
  • Cell Biology

Background:

  • Microparticles are cell-derived vesicles implicated in procoagulant and proinflammatory processes.
  • Cell activation, including apoptosis, releases microparticles that may influence vascular function.

Purpose of the Study:

  • To investigate the impact of microparticles on vascular reactivity.
  • To elucidate the mechanisms underlying microparticle-induced vascular effects.

Main Methods:

  • Assessed vascular reactivity in mouse aorta exposed to microparticles from apoptotic T cells or diabetic patients.
  • Utilized nitric oxide (NO) synthase and cyclooxygenase-2 inhibitors to evaluate the role of these pathways.
  • Examined proinflammatory protein expression and NF-kappaB activation via immunochemical staining and pathway analysis.
  • Investigated in vivo effects of lymphocyte-derived microparticles in mice.

Main Results:

  • Microparticles induced vascular hyporeactivity to vasoconstrictors in mouse aorta.
  • This hyporeactivity was reversed by NO synthase and cyclooxygenase-2 inhibitors.
  • Associated with increased production of vasodilatory products (NO, prostacyclin) and upregulation of inducible NO-synthase and cyclooxygenase-2.
  • Microparticles activated NF-kappaB, potentially via the Fas/Fas Ligand pathway.
  • In vivo treatment with microparticles caused reversible vascular hyporeactivity.

Conclusions:

  • Microparticles act as vectors in transcellular signaling, contributing to vascular dysfunction.
  • These findings offer a mechanistic explanation for the role of microparticles in inflammatory diseases and vascular complications.

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