Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

Dong, Jian; Zhu, Hai; Zhu, Wei; Ding, Hai; Min, Tie; Zhou, Zhao Nian

doi:10.1038/sj.cr.7290184

Cited by 117 publications

(84 citation statements)

References 35 publications

(50 reference statements)

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“…5B). Therefore, our findings support previous data suggesting that ischemia and reperfusion induces myocardial cell apoptosis (31,50,51) that is mediated by PKC␦ translocation to the mitochondria and the activation of the apoptotic effectors involving cytochrome c release, caspase 3 activation, PARP cleavage, and DNA fragmentation. …”

Section: ␦V1-1 Inhibits Pkc␦ Translocation During Reperfusion-wesupporting

confidence: 81%

Protein Kinase Cδ Activation Induces Apoptosis in Response to Cardiac Ischemia and Reperfusion Damage

Murriel

Churchill

Inagaki

et al. 2004

Journal of Biological Chemistry

185

148

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Heart attacks caused by occlusion of coronary arteries are often treated by mechanical or enzymatic removal of the occlusion and reperfusion of the ischemic heart. It is now recognized that reperfusion per se contributes to myocardial damage, and there is a great interest in identifying the molecular basis of this damage. We recently showed that inhibiting protein kinase C␦ (PKC␦) protects the heart from ischemia and reperfusion-induced damage. Here, we demonstrate that PKC␦ activity and mitochondrial translocation at the onset of reperfusion mediates apoptosis by facilitating the accumulation and dephosphorylation of the pro-apoptotic BAD (Bcl-2-associated death promoter), dephosphorylation of Akt, cytochrome c release, PARP (poly(ADPribose) polymerase) cleavage, and DNA laddering. Our data suggest that PKC␦ activation has a critical proapoptotic role in cardiac responses following ischemia and reperfusion.

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Section: ␦V1-1 Inhibits Pkc␦ Translocation During Reperfusion-wesupporting

confidence: 81%

Protein Kinase Cδ Activation Induces Apoptosis in Response to Cardiac Ischemia and Reperfusion Damage

Murriel

Churchill

Inagaki

et al. 2004

Journal of Biological Chemistry

185

148

View full text Add to dashboard Cite

show abstract

“…In addition, it was found that prolonged intermittent hypoxic exposure induces myocardial tolerance against H/R injury in association with an elevation of Bcl-2 protein level through NF-kB activation. This possibility is supported by recent studies that indicated that Bcl-2 overexpression limits apoptosis in I/R injury of heart and liver [28]. It is known that the relationship between p53 and ROS is multifactorial [11,13,18].…”

Section: 5supporting

confidence: 72%

“…Fluorescence, arbitrary units Bcl-2 and Bcl-xl result in marked disruption of mitochondrial membranes and subsequent cytochrome c release and procaspase-3 activation [28]. In our study, short-term H/R resulted in a remarkable rise in ROS formation as well as in the induction of p53 protein content that was associated with a decrease in Bcl-2 protein level in mitochondria (Fig.…”

Section: 5mentioning

confidence: 57%

“…Although the fact of apoptosis induction during hypoxia was confirmed in several independent studies [19,28], the exact mechanisms of this effect remain unknown. It was reported that the Hif-1 gene overexpression might play a trigger role in this pro- Bcl-2 → β-actin → cess because Hif-1α can bind to the p53 and promote p53-dependent apoptosis [29].…”

Section: 5mentioning

confidence: 98%

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Changes in proHB-EGF expression after functional activation of the immune system cells

Gonchar¹,

Mankovskaya²

2017

Ukr.Biochem.J.

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The intensity of oxidative stress, protein expression of antiapoptotic Bcl-2 as well as antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase (GPx) and their regulator p53 were studied in the mitochondria of rat heart. Sessions of repeated hypoxia/reoxygenation ((h/r) A large body of experimental data indicates that reactive oxygen species (ROS) play a fundamental role in hypoxia/reoxygenation injury of cells and subcellular structures [1]. Mitochondria are considered an important locus of ROS production mainly at the level of complexes I and III of the respiratory chain and hence a potential contributor to cells damage during hypoxia [2]. At the same time, mitochondria could be major targets of ROS attack. These events result in mitochondrial dysfunction with superoxide leakage, the formation of other aggressive ROS which attack lipids, proteins and other cell constituents, lead to energy and metabolic disorders, deplete of cellular antioxidant defense, and induce the apoptotic cascade [1,2].In general, mitochondrial oxidative stress is determined by the balance between ROS generation and their elimination by antioxidants [3]. The antioxidants and free radical scavenging enzymes, including MnSOD, peroxiredoxin 3 and 5, thioredoxin, glutathione, and glutathione peroxidase, not only constitute the first line of defense against oxidative damage within the mitochondria but also are essential for maintaining the critical cellular redox balance and play key role in modulating cellular responses to external stimuli [4]. MnSOD and GPxthe key antioxidant defense enzymes that function in concert to prevent ROS reactions in response to oxidative stress [5]. There are plenty of reports concerning the role of MnSOD and GPx in the cellular redox homeostasis involved in the adaptive responses against oxidative stress [6][7][8][9], although the mechanisms associated with protein expression and specific activity of MnSOD as well as GPx during H/R of different duration are not fully understood.

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“…Similarly, hypoxic pretreatment can also protect other tissues like heart or brain against various toxic insults (Gidday et al 1994;Emerson et al 1999;Cai et al 2003;Dong et al 2003) suggesting that hypoxic preconditioning might induce a general protective response. Such a response might involve hypoxia-inducible-factor 1a which is stabilized in the retina after hypoxic exposure (Grimm et al 2002).…”

Section: Introductionmentioning

confidence: 99%

The Hypoxic Transcriptome of the Retina: Identification of Factors with Potential Neuroprotective Activity

Thiersch

Raffelsberger

Frigg

et al. 2008

Advances in Experimental Medicine and Biology

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Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

Cited by 117 publications

References 35 publications

Protein Kinase Cδ Activation Induces Apoptosis in Response to Cardiac Ischemia and Reperfusion Damage

Protein Kinase Cδ Activation Induces Apoptosis in Response to Cardiac Ischemia and Reperfusion Damage

Changes in proHB-EGF expression after functional activation of the immune system cells

The Hypoxic Transcriptome of the Retina: Identification of Factors with Potential Neuroprotective Activity

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