Proteasome inhibition ablates activation of NF-kappa B in myocardial reperfusion and reduces reperfusion injury.
@article{Pye2003ProteasomeIA,
title={Proteasome inhibition ablates activation of NF-kappa B in myocardial reperfusion and reduces reperfusion injury.},
author={J. Philip Pye and Farhad Ardeshirpour and Arlene S McCain and Dwight A. Bellinger and Elizabeth P. Merricks and Julian Robert James Adams and Peter J. Elliott and Christine Pien and Thomas H. Fischer and Albert S. Baldwin and Timothy C. Nichols},
journal={American journal of physiology. Heart and circulatory physiology},
year={2003},
volume={284 3},
pages={
H919-26
}
}Both acute coronary occlusion and reperfusion of an infarct-related artery lead to significant myocardial cell death. Recent evidence has been presented that activation of the transcription factor nuclear factor-kappaB (NF-kappaB) plays a critical role in reperfusion injury. NF-kappaB is usually bound to its inhibitor, IkappaB, and classic activation of NF-kappaB occurs when the 20S proteasome degrades IkappaB that has been phosphorylated and ubiquitinated. In this study, activation of NF…
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References
SHOWING 1-10 OF 43 REFERENCES
Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide
- Biology
- 2000
It is reported here that a naturally occurring antibacterial peptide PR39 reversibly binds to the alpha 7 subunit of the 26S proteasome and blocks degradation of NF-kappa B inhibitor I kappa B alpha by the ubiquitin-proteasome pathway without affecting overall proteasomes activity.
Inhibition of ubiquitin-proteasome pathway-mediated I kappa B alpha degradation by a naturally occurring antibacterial peptide.
- BiologyThe Journal of clinical investigation
- 2000
It is reported here that a naturally occurring antibacterial peptide PR39 reversibly binds to the alpha 7 subunit of the 26S proteasome and blocks degradation of NF-kappa B inhibitor I kappa B alpha by the ubiquitin-proteasome pathway without affecting overall proteasomes activity.
Inhibition of interleukin-8 blocks myocardial ischemia-reperfusion injury.
- Biology, MedicineThe Journal of thoracic and cardiovascular surgery
- 1998
Role of mitogen-activated protein kinases in ischemia and reperfusion injury : the good and the bad.
- BiologyCirculation research
- 2000
A new study by Yue et al1 in this issue of Circulation Research attempts to address the role of MAP kinases in ischemic myocardium and suggests that ERK1/ERK2 is part of a “survival” pathway whereas p38 and JNK mediate a ‘death’ pathway in the ischems of the heart.
Apoptosis is initiated by myocardial ischemia and executed during reperfusion.
- Biology, MedicineJournal of molecular and cellular cardiology
- 2000
It is concluded that cell death in acute global ischemia followed by reperfusion occurs predominantly by necrosis and that apoptosis is of minor importance in this pathophysiological situation.
Cardioprotective effects of a novel proteasome inhibitor following ischemia and reperfusion in the isolated perfused rat heart.
- Biology, MedicineJournal of molecular and cellular cardiology
- 1999
Evidence is provided that PS-519 is a potent and effective cardioprotective agent that inhibits P-selectin leukocyte-endothelial cell interactions and preserves cardiac contractile function and coronary perfusion following myocardial ischemia and reperfusion.
Co-localization of the cysteine protease caspase-3 with apoptotic myocytes after in vivo myocardial ischemia and reperfusion in the rat.
- BiologyJournal of molecular and cellular cardiology
- 1998
TUNEL staining of formalin-fixed, paraffin-embedded left ventricle, and DNA fragmentation analysis, showed that apoptosis occurred during 45 min of ischemia alone, but further developed during the 3-h reperfusion period, which implicate caspase-3 to be involved in apoptotic cell death in ischemic/reperfused rat heart.
Reperfusion induces myocardial apoptotic cell death.
- Biology, MedicineCardiovascular research
- 2000
Inhibition versus induction of apoptosis by proteasome inhibitors depends on concentration
- Biology, ChemistryCell Death and Differentiation
- 1998
The results suggest that the pro-APoptotic and anti-apoptotic functions of peptide aldehyde proteasome inhibitors such as MG-132 depend on the concentration of inhibitor utilized and expand the list of stimuli requiring proteasomal activation to induce apoptosis to include viruses.
In vivo transfection of cis element “decoy” against nuclear factor- κB binding site prevents myocardial infarction
- BiologyNature Medicine
- 1997
The first successful in vivo transfer of NFκB decoy oligodeoxynucleotides to reduce the extent of myocardial infarction following reperfusion is reported, providing a new therapeutic strategy for myocardia infarctions.






