Proteomic and metabolomic analysis of atrial profibrillatory remodelling in congestive heart failure

Souza, Ayesha I. De; Cardin, Sophie; Wait, Robin; Chung, Yuen‐Li; Vijayakumar, Meeraa; Maguy, Ange; Camm, A. John; Nattel, Stanley

doi:10.1016/j.yjmcc.2010.07.008

Cited by 82 publications

(81 citation statements)

References 54 publications

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“…Increase of myocardial HSP60 was also found in a model of HF induced by coronary artery ligation in rats [39] as well as in a model of HF induced in ventricular-tachypaced dogs [40]. Subsequent work with a rat model showed that treatment with trandolapril reversed the HSP60 increases [41].…”

Section: Hsp60 and The Pathogenesis Of Heart Failure (Hf) And Hypertementioning

confidence: 80%

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecular chaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60, the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotective but a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examples of specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicate a pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response to treatment, as well as for preventing and treating CVD.

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Section: Hsp60 and The Pathogenesis Of Heart Failure (Hf) And Hypertementioning

confidence: 80%

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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“…22 Another proteomics and metabolomics analysis found that malate dehydrogenase, the α-subunit of the E1 component of pyruvate-DH, and α-and β-enolase expression were increased at 24-h and decreased at 2-week ventricular tachypacing. 23 Those changes were related to the congestive heart failure-associated atrial remodeling and suggested that metabolic remodeling may contribute to the AF substrate. 23 α-enolase is also downregulated in human permanent AF.…”

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confidence: 99%

“…23 Those changes were related to the congestive heart failure-associated atrial remodeling and suggested that metabolic remodeling may contribute to the AF substrate. 23 α-enolase is also downregulated in human permanent AF. 24 Thus, early increased expression is likely a response to increased metabolic needs, and longer-term decreased expression, an energy-saving adaptation.…”

mentioning

confidence: 99%

Quantitative Proteomics of Changes in Energy Metabolism-Related Proteins in Atrial Tissue From Valvular Disease Patients With Permanent Atrial Fibrillation

Zhou

Liu

et al. 2014

Circ J

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“…The actin-capping, aggregation and, possibly molecular chaperone function, of hsp27 are regulated by phosphorylation (see [8,10]). The expression and/or phosphorylation of hsp27 in the heart is increased in response to chronic pressure overload [20], both physiological and pathological hypertrophy [13], heart failure [21,38,39], oxidative stress [24,25], ischemic injury [22], and haemorrhagic shock [23]. Increased hsp27 expression prevents cardiac dysfunction and hypertrophy during chronic pressure overload [13], protects against doxorubicin-induced cardiomyopathy [26,27], and prevents tachypacing-induced atrial remodelling and atrial fibrillation [14,17,16,19].…”

Section: Discussionmentioning

confidence: 99%

Characterization of hsp27 kinases activated by elevated aortic pressure in heart

et al. 2012

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Chronic hemodynamic overload results in left ventricular hypertrophy, fibroblast proliferation, and interstitial fibrosis. The small heat shock protein hsp27 has been shown to be cardioprotective and this requires a phosphorylatable form of this protein. To further understand the regulation of hsp27 in heart in response to stress, we investigated the ability of elevated aortic pressure to activate hsp27-kinase activities. Isolated hearts were subjected to retrograde perfusion and then snapfrozen. Hsp27-kinase activity was measured in vitro as hsp27 phosphorylation. Immune complex assays revealed that MK2 activity was low in non-perfused hearts and increased following crystalline perfusion at 60 or 120 mmHg. Hsp27-kinase activities were further studied following ion-exchange chromatography. Anion exchange chromatography on Mono Q revealed 2 peaks ('b' and 'c') of hsp27-kinase activity. A third peak 'a' was detected upon chromatography of the Mono Q flow-through fractions on the cation exchange resin, Mono S. The hsp27-kinase activity underlying peaks 'a' and 'c' increased as perfusion pressure was increased from 40 to 120 mmHg. In contrast, peak 'b' increased over pressures 60-100 mmHg but was decreased at 120 mmHg. Peaks 'a', 'b', and 'c' contained MK2 immunoreactivity, whereas MK3 and MK5 immunoreactivity was detected in peak 'a'. p38 MAPK and phospho-p38 MAPK were also detected in peaks 'b' and 'c' but absent from peak 'a'. Hsp27-kinase activity in peaks 'b' and 'c' (120 mmHg) eluted from a Superose 12 gel filtration column with an apparent molecular mass of 50-kDa. Hence, peaks 'b' and 'c' were not a result of MK2 forming complexes. In-gel hsp27-kinase assays revealed a single 49-kDa renaturable hsp27-kinase activity in peaks 'b' and 'c' at 60 mmHg, whereas several hsp27-kinases (p43, p49, p54, p66) were detected in peaks 'b' and 'c' from hearts perfused at 120 mmHg. Thus, multiple hsp27-kinases were activated in response to elevated aortic pressure in isolated, perfused rat hearts and hence may be implicated in regulating the cardioprotective effects of hsp27 and thus may represent targets for cardioprotective therapy.

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Proteomic and metabolomic analysis of atrial profibrillatory remodelling in congestive heart failure

Cited by 82 publications

References 54 publications

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Quantitative Proteomics of Changes in Energy Metabolism-Related Proteins in Atrial Tissue From Valvular Disease Patients With Permanent Atrial Fibrillation

Characterization of hsp27 kinases activated by elevated aortic pressure in heart

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