Suppression of proteasome C2 contralateral to ischemic lesions in rat brain

Keyvani, Kathy; Reinecke, Sonja; Abts, Harry F.; Paulus, Werner; Witte, Otto W.

doi:10.1016/s0006-8993(00)01978-8

Cited by 14 publications

(9 citation statements)

References 37 publications

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“…The first evidence for dysfunction of the proteasome during ischemia is derived from the neurology literature. At least three studies demonstrate inhibition of the 20S proteasome in stroke models associated with accumulation of oxidized and ubiquitinated proteins (10,114,119). The earliest evidence of decreased proteasome function in myocardial ischemia was presented by Bulteau et al (21), who showed loss of non-ATP dependent (20S proteasome) trypsinlike activity after 30 min of in vivo LAD occlusion.…”

Section: Proteasome Dysfunction In Myocardial Ischemiamentioning

confidence: 99%

The ubiquitin-proteasome system in cardiac physiology and pathology

Powell

2006

American Journal of Physiology-Heart and Circulatory Physiology

146

118

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The ubiquitin-proteasome system (UPS) is the major nonlysosomal pathway for intracellular protein degradation, generally requiring a covalent linkage of one or more chains of polyubiquitins to the protein intended for degradation. It has become clear that the UPS plays major roles in regulating many cellular processes, including the cell cycle, immune responses, apoptosis, cell signaling, and protein turnover under normal and pathological conditions, as well as in protein quality control by removal of damaged, oxidized, and/or misfolded proteins. This review will present an overview of the structure, biochemistry, and physiology of the UPS with emphasis on its role in the heart, if known. In addition, evidence will be presented supporting the role of certain muscle-specific ubiquitin protein ligases, key regulatory components of the UPS, in regulation of sarcomere protein turnover and cardiomyocyte size and how this might play a role in induction of the hypertrophic phenotype. Moreover, this review will present the evidence suggesting that proteasomal dysfunction may play a role in cardiac pathologies such as myocardial ischemia, congestive heart failure, and myofilament-related and idiopathic-dilated cardiomyopathies, as well as cardiomyocyte loss in the aging heart. Finally, certain pitfalls of proteasome studies will be described with the intent of providing investigators with enough information to avoid these problems. This review should provide current investigators in the field with an up-to-date analysis of the literature and at the same time provide an impetus for new investigators to enter this important and rapidly changing area of research.

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Section: Proteasome Dysfunction In Myocardial Ischemiamentioning

confidence: 99%

The ubiquitin-proteasome system in cardiac physiology and pathology

Powell

2006

American Journal of Physiology-Heart and Circulatory Physiology

146

118

View full text Add to dashboard Cite

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“…Other groups also have used this technique in ischemia to identify differentially expressed mRNA such as serine protease inhibitors (SPI-3), zinc transporter gene (ZnT-1), and ADP-ribosylation factor like gene (ARF4L) in models of gerbil forebrain ischemia (Tsuda et al, 1996(Tsuda et al, , 1997Katayama et al, 1998). Proteosome expression was identified after rat photochemical ischemia (Keyvani et al, 2000). Transcription factor (SEF-2) and proteosome expression (p112) after rat global ischemia (Wigle et al, 1999) and chemokine identification (ST-38) after rat MCAO (Utans-Schneitz et al, 1998) also were demonstrated.…”

Section: Differential Displaymentioning

confidence: 99%

Stroke Genomics: Approaches to Identify, Validate, and Understand Ischemic Stroke Gene Expression

Read

Parsons

Harrison

et al. 2001

J Cereb Blood Flow Metab

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Sequencing of the human genome is nearing completion and biologists, molecular biologists, and bioinformatics specialists have teamed up to develop global genomic technologies to help decipher the complex nature of pathophysiologic gene function. This review will focus on differential gene expression in ischemic stroke. It will discuss inheritance in the broader stroke population, how experimental models of spontaneous stroke might be applied to humans to identify chromosomal loci of increased risk and ischemic sensitivity, and also how the gene expression induced by stroke is related to the poststroke processes of brain injury, repair, and recovery. In addition, we discuss and summarise the literature of experimental stroke genomics and compare several approaches of differential gene expression analyzes. These include a comparison of representational difference analysis we have provided using an experimental stroke model that is representative of stroke evolution observed most often in man, and a summary of available data on stroke differential gene expression. Issues regarding validation of potential genes as stroke targets, the verification of message translation to protein products, the relevance of the expression of neuroprotective and neurodestructive genes and their specific timings, and the emerging problems of handling novel genes that may be discovered during differential gene expression analyses will also be addressed.

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“…Yet the prospective roles of the proteasomes in cell death or recovery during myocardial ischemia have not been examined in any great detail. Most of the studies of proteasome in ischemic injury are in nervous tissue and demonstrate inhibition of the 20S proteasome associated with accumulation of oxidized and ubiquitinated proteins (2,21,22). One study in the heart (5) has demonstrated oxidative modification and inactivation of the 20S proteasome following 30 min of left anterior descending artery occlusion.…”

Section: Introductionmentioning

confidence: 99%

Oxidized and Ubiquitinated Proteins May Predict Recovery of Postischemic Cardiac Function: Essential Role of the Proteasome

Powell

Wang²,

Katzeff³

et al. 2005

Antioxidants & Redox Signaling

117

103

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This study examined the hypothesis that postischemic levels of oxidized and/or ubiquitinated proteins may be predictive of functional recovery as they may be indicative of activity of the 20S and/or 26S proteasomes, respectively. Subjecting isolated rat hearts to 15 min of ischemia had no effect on 20S- and 26S-proteasome activities; however, both were significantly (p < 0.05) decreased by 70% and 54%, respectively, following 30 min of ischemia and 60 min of reperfusion, changes associated with increased levels of protein carbonyls and ubiquitinated proteins. Preischemic treatment of hearts with the proteasome inhibitor, MG132, resulted in dose-dependent decreases (p < 0.05) in recovery of postischemic function [MG132 (microM), heart rate x pressure product: 0, 11,158 +/- 2,423; 6, 11,400 +/- 3,009; 12, 5,513 +/- 2,225; 25, 2,325 +/- 992] and increased accumulation of ubiquitinated proteins. Preconditioning with repetitive ischemia (IP) or preischemic treatment with nicorandil (Nic) resulted in a significant increase in postischemic 20S-proteasome activity after 60 min of reperfusion (control, 95 +/- 4; IP, 301 +/- 65; Nic, 242 +/- 61 fluorescence units). Only Nic had similar effects on 26S-proteasome activity. These results support the conclusion that a correlation exists between eventual recovery of postischemic function and levels of oxidized and/or ubiquitinated proteins, a phenomenon that may be dependent on activity of the 20S and 26S proteasomes.

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Suppression of proteasome C2 contralateral to ischemic lesions in rat brain

Cited by 14 publications

References 37 publications

The ubiquitin-proteasome system in cardiac physiology and pathology

The ubiquitin-proteasome system in cardiac physiology and pathology

Stroke Genomics: Approaches to Identify, Validate, and Understand Ischemic Stroke Gene Expression

Oxidized and Ubiquitinated Proteins May Predict Recovery of Postischemic Cardiac Function: Essential Role of the Proteasome

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