Apoptosis in pressure overload-induced heart hypertrophy in the rat.

Teiger, Emmanuel; Than, V D; Richard, Lucie; Wisnewsky, C; Tea, Bun-Seng; Gaboury, Louis; Tremblay, Johanne; Schwartz, Kenneth S.; Hamet, Pavel

doi:10.1172/jci118747

Cited by 387 publications

(187 citation statements)

References 25 publications

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“…Thus, the rate of apoptosis in normal human heart is B1 per 10 000 cardiomyocytes, but apoptosis increases several hundred-fold in ischemic and dilated cardiomyopathy and reactive cardiac hypertrophy (Narula et al, 1996;Teiger et al, 1996;Olivetti et al, 1997). Because adult cardiac myocytes are incapable of meaningful cellular regeneration (Rubart and Field, 2006), chronic persistent apoptosis at a rate of 0.1-1% of total cardiomyocytes, as is observed in human cardiomyopathies, may be sufficient to produce cardiac dilation and heart failure (Hayakawa et al, 2003).…”

Section: Cardiomyocyte Apoptosis and Bcl2 Proteins In Myocardial Diseasementioning

confidence: 99%

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Dorn

Kirshenbaum

2008

Oncogene

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Programmed cardiac myocyte death contributes to pathological ventricular remodeling and the progression of myocardial infarction or pressure overload hypertrophy to dilated cardiomyopathy. Recent work has identified importance of stress-mediated transcriptional induction of BNIP3 (BCL2 and 19-kDa interacting protein-3) and NIX/BNIP3L in cardiac remodeling. Here, the regulatory mechanisms for these two factors in the heart and their effects on programmed cardiomyocyte death are reviewed, with a focus on information derived from studies using mouse models of cardiac BNIP3 and NIX/BNIP3L overexpression and gene ablation.

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Section: Cardiomyocyte Apoptosis and Bcl2 Proteins In Myocardial Diseasementioning

confidence: 99%

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Dorn

Kirshenbaum

2008

Oncogene

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“…Apoptosis occurs in the myocardium of patients with end-stage heart failure and myocardial infarction (MI), and in animal models of myocardial hypertrophy and failure [1][2][3]. Stimulation of β-adrenergic receptor (β-AR) induces apoptosis in cardiac myocytes in vitro and in vivo [4].…”

Section: Introductionmentioning

confidence: 99%

Glycogen synthase kinase-3β plays a pro-apoptotic role in β-adrenergic receptor-stimulated apoptosis in adult rat ventricular myocytes: Role of β1 integrins

Menon

Johnson

Ross

et al. 2007

Journal of Molecular and Cellular Cardiology

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Abstractβ-adrenergic receptor (β-AR) stimulation induces apoptosis in adult rat ventricular myocytes (ARVM). β1 integrin signaling plays a protective role in β-AR-stimulated apoptosis. Glycogen synthase kinase-3β (GSK-3β), a multifunctional serine/threonine kinase, negatively regulates cardiac hypertrophy. Here we show that β-AR stimulation (isoproterenol; 15 min) increases tyr 216 phosphorylation and GSK-3β activity. Inclusion of LiCl, inhibitor of GSK-3β, in the reaction mix or expression of catalytically inactive GSK-3β (KM-GSK) inhibited β-AR-stimulated GSK-3β activity. Inhibition of tyrosine kinase using genistein or chelation of intracellular Ca 2+ using BAPTA-AM inhibited β-AR-stimulated increases in tyr 216 phosphorylation and GSK-3β activity. Inhibition of GSK-3β using pharmacological inhibitors or infection with KM-GSK decreased β-AR-stimulated cytosolic cytochrome C release and apoptosis. Expression of β1 integrins increased ser 9 phosphorylation and inhibited β-AR-stimulated increase in GSK-3β activity. Wortmannin, inhibitor of PI3-kinase, reversed the effects of β1 integrins on GSK-3β activity and apoptosis. Purified active matrix metalloproteinase-2 (MMP-2), shown to interfere with β1 integrin signaling, increased GSK-3β activity, while inhibition of MMP-2 inhibited β-AR-stimulated increases in GSK-3β activity. β-AR stimulation induced nuclear accumulation of GSK-3β. β-AR stimulation (3 h) increased the expression of transcription factor Gadd153 (growth arrest-and DNA damage-inducible gene 153). These data suggest that β-AR stimulation increases GSK-3β activity. Activation of GSK-3β plays a pro-apoptotic role in β-AR stimulated apoptosis via the involvement of mitochondrial death pathway. β1 integrins inactivate GSK-3β and play an anti-apoptotic role via the involvement of PI3-kinase pathway. The apoptotic effects of GSK-3β may be mediated, at least in part, via its nuclear localization and induction of pro-apoptotic genes, such as Gadd153.

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“…36 Noticeably, this cytoprotective effect may be weakened in hypertrophic heart because miR-133 levels have been found to be significantly reduced under such conditions and this may contribute to the increased tendency for the induction of apoptosis in hypertrophic myocytes. [37][38][39] Our study demonstrated that miR-1, another muscle-specific miRNA, promotes apoptosis induced by oxidative stress in cardiac cells and counteracts the effects of miR-133. 36 Intriguingly, an earlier study revealed that miR-1 levels are elevated by two-to threefold in ischaemic myocardium.…”

Section: How Many Mirnas Can Affect Apoptosis?mentioning

confidence: 64%

MicroRNAs and apoptosis: implications in the molecular therapy of human disease

Yang

Wang

2009

Clin Exp Pharma Physio

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SUMMARY1. MicroRNAs (miRNAs), the small non-coding RNAs of approximately 22 nucleotides, are now recognized as a very large family present throughout the genomes of plants and metazoans. These small transcripts modulate protein expression by binding to complementary or partially complementary target proteincoding mRNAs and targeting them for degradation or translational inhibition.2. The discovery of miRNAs has revolutionized our understanding of the mechanisms that regulate gene expression, with the addition of an entirely novel level of regulatory control. Considerable information on miRNAs has been accumulated in this rapidly evolving research field. We now know that miRNAs play pivotal roles in diverse processes, such as development and differentiation, control of cell proliferation and death, stress response and metabolism. Indeed, aberrant miRNA expression has been documented in human disease as well as in animal models, with evidence for a causative role in tumourigenesis.3. One of the most active fields of miRNA research is miRNA regulation of apoptosis, a programmed cell death implicated in many human diseases, such as cancer, Alzheimer's disease, hypertrophy and heart failure. Thus far, nearly 30 of 500 human miRNAs have been validated experimentally to regulate apoptosis; this number is likely to increase with future studies.4. The present review provides a comprehensive summary and analysis of the currently available data, focusing on the transcriptional controls, target genes and signalling pathways linking the apoptosis-regulating miRNAs and apoptotic cell death.

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Apoptosis in pressure overload-induced heart hypertrophy in the rat.

Cited by 387 publications

References 25 publications

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

Glycogen synthase kinase-3β plays a pro-apoptotic role in β-adrenergic receptor-stimulated apoptosis in adult rat ventricular myocytes: Role of β1 integrins

MicroRNAs and apoptosis: implications in the molecular therapy of human disease

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