Carbon monoxide suppresses arteriosclerotic lesions associated with chronic graft rejection and with balloon injury. Academic Article uri icon

Overview

MeSH

  • Animals
  • Cyclic GMP
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Enzyme Activation
  • Guanylate Cyclase
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitogen-Activated Protein Kinases
  • Nitric Oxide Synthase
  • Rats
  • Rats, Sprague-Dawley
  • p38 Mitogen-Activated Protein Kinases

MeSH Major

  • Angioplasty, Balloon, Coronary
  • Arteriosclerosis
  • Carbon Monoxide
  • Graft Rejection

abstract

  • Carbon monoxide (CO), one of the products of heme oxygenase action on heme, prevents arteriosclerotic lesions that occur following aorta transplantation; pre-exposure to 250 parts per million of CO for 1 hour before injury suppresses stenosis after carotid balloon injury in rats as well as in mice. The protective effect of CO is associated with a profound inhibition of graft leukocyte infiltration/activation as well as with inhibition of smooth muscle cell proliferation. The anti-proliferative effect of CO in vitro requires the activation of guanylate cyclase, the generation of cGMP, the activation of p38 mitogen-activated protein kinases and the expression of the cell cycle inhibitor p21Cip1. These findings demonstrate a protective role for CO in vascular injury and support its use as a therapeutic agent.

publication date

  • February 2003

has subject area

  • Angioplasty, Balloon, Coronary
  • Animals
  • Arteriosclerosis
  • Carbon Monoxide
  • Cyclic GMP
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Enzyme Activation
  • Graft Rejection
  • Guanylate Cyclase
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitogen-Activated Protein Kinases
  • Nitric Oxide Synthase
  • Rats
  • Rats, Sprague-Dawley
  • p38 Mitogen-Activated Protein Kinases

Research

keywords

  • Journal Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1038/nm817

PubMed ID

  • 12539038

Additional Document Info

start page

  • 183

end page

  • 190

volume

  • 9

number

  • 2