Proteasome mediates removal of proteins oxidized during myocardial ischemia

Numerous proteins are known to be lost following myocardial ischemia/reperfusion yet little is known about the mediating proteinases. This study examines the hypothesis that proteasome plays a significant role in the removal of proteins oxidized during myocardial ischemia. Proteasome was inhibited b...

Full description

Saved in:
Bibliographic Details
Published in:Free radical biology & medicine 2006, Vol.40 (1), p.156-164
Main Authors: Divald, Andras, Powell, Saul R.
Format: Article
Language:English
Subjects:
3-Methylhistidine
Acetylcysteine - analogs & derivatives
Acetylcysteine - pharmacology
Actin
Actins - metabolism
Animals
Cysteine Proteinase Inhibitors - pharmacology
Free radical
Heart - physiopathology
Immunoprecipitation
Ischemic Preconditioning, Myocardial
Male
Methylhistidines - metabolism
Myocardial ischemia
Myocardial Ischemia - metabolism
Myocardial Ischemia - pathology
Oxidation-Reduction
Proteasome
Proteasome Endopeptidase Complex - metabolism
Proteasome Inhibitors
Protein oxidation
Proteins - metabolism
Rats
Rats, Sprague-Dawley
Reperfusion
Ubiquitin - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Numerous proteins are known to be lost following myocardial ischemia/reperfusion yet little is known about the mediating proteinases. This study examines the hypothesis that proteasome plays a significant role in the removal of proteins oxidized during myocardial ischemia. Proteasome was inhibited by perfusing isolated rat hearts with buffer containing lactacystin, 2 μmol/L, for 10 min, which resulted in 51 and 42% decreases in 20S and 26S proteasome activities that persisted for a minimum of 90 min. Lactacystin pretreatment had minor effects on postischemic recovery of isolated hearts exposed to 30 min global ischemia and 60 min reperfusion. Protein carbonyl content of lactacystin-pretreated ischemic hearts was significantly ( P 
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2005.09.022