Ischemic Preconditioning in Isolated Cells

Marber, Michael

doi:10.1161/01.res.86.9.926

Cited by 48 publications

(42 citation statements)

References 47 publications

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“…As described previously (23,35), preconditioning was created by placing the cultured neonatal rat ventricular cardiomyocytes in a hypoxic chamber (1% O 2, 5% CO2; 37°C) for 3 h and then returned to control conditions (21% O2, 5% CO2; 37°C) for 24 h, followed by simulated lethal ischemia (depletion of serum and glucose and hypoxia) for 2 h. The cardiomyocyte cultures were then maintained under control conditions for an additional 15 h. The cellular level of 3-(4,5-dimethylthiazol-2-yl-5)-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS), indicative of the mitochondrial function in living cells and cell viability, and lactate dehydrogenase (LDH) levels in the culture medium were measured with the CellTiter96 Aqueous One kit (Promega) and the TOX-7 assay kit (Sigma), respectively (11).…”

Section: Methodsmentioning

confidence: 99%

“…We also measured the cellular protein levels of HIF-1␣ and the mRNA levels of several HIF-1 target genes in a cultured neonatal rat cardiomyocyte model of preconditioning (2,13,23,28,35,38). Our results suggest that expression of a constitutively stable hybrid HIF-1␣ protects cultured neonatal cardiomyocytes against simulated ischemia-reperfusion injury by inducing multiple protective genes.…”

mentioning

confidence: 86%

“…NO plays a dual role in the pathophysiology of the late phase of preconditioning (8,23). Enhanced biosynthesis of NO by eNOS is essential to trigger the late phase of ischemia-induced or exercise-induced preconditioning.…”

Section: Fig 1 Effects Of Preconditioning (Pc) On Cell Viability (Amentioning

confidence: 99%

“…An early phase of protection that develops within minutes after the preconditioning stimulus lasts for 2-3 h, whereas a late phase of protection that occurs 12-24 h later lasts for 3-4 days (8,21,23). A number of chemical signals that trigger the development of the late phase of preconditioning, including adenosine, NO, reactive oxygen species, and opioid receptor agonists, have been identified (8,23). Activation of protein kinase C (4), protein tyrosine kinases (16), and mitogen-activated protein kinases (33) by these triggers leads to increased expression of the mediators of the late phase of preconditioning.…”

mentioning

confidence: 99%

“…Activation of protein kinase C (4), protein tyrosine kinases (16), and mitogen-activated protein kinases (33) by these triggers leads to increased expression of the mediators of the late phase of preconditioning. Myocardial protein synthesis of several mediators (or effectors), including inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), aldose reductase, antioxidant enzymes, and heat shock proteins (HSPs), and activation of ATP-sensitive K ϩ (K ATP ) channels play a critical role in late-phase preconditioning (8,15,21,23,24,29). It has been proposed that activator protein 1 (AP-1) and nuclear factor-B (NF-B) may mediate the transcriptional activation of iNOS, COX-2, aldose reductase, and other genes (22,36).…”

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confidence: 99%

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Expression of constitutively stable hybrid hypoxia-inducible factor-1α protects cultured rat cardiomyocytes against simulated ischemia-reperfusion injury

Date¹,

Mochizuki²,

Belanger³

et al. 2005

American Journal of Physiology-Cell Physiology

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 86%

Section: Fig 1 Effects Of Preconditioning (Pc) On Cell Viability (Amentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Expression of constitutively stable hybrid hypoxia-inducible factor-1α protects cultured rat cardiomyocytes against simulated ischemia-reperfusion injury

Date¹,

Mochizuki²,

Belanger³

et al. 2005

American Journal of Physiology-Cell Physiology

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Combined hypoxia and sodium nitrite pretreatment for cardiomyocyte protection in vitro

Hsieh

Feric

Radišić

2015

Biotechnology Progress

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Methods that increase cardiomyocyte survival upon exposure to ischemia, hypoxia and reoxygenation injuries are required to improve the efficacy of cardiac cell therapy and enhance the viability and function of engineered tissues. We investigated the effect of combined hypoxia/NaNO2 pretreatment on rat neonatal cardiomyocyte (CM), cardiac fibroblast, and human embryonic stem cell-derived CM (hESC-CM) survival upon exposure to hypoxia/reoxygenation (H/R) injury in vitro. Cells were pretreated with and without hypoxia and/or various concentrations of NaNO2 for 20 min, then incubated for 2 h under hypoxic conditions, followed by 2 h in normoxia. The control cells were maintained under normoxia for 4 h. Pretreatment with either hypoxia or NaNO2 significantly increased CM viability but had no effect on cardiac fibroblast viability. Combined hypoxia/NaNO2 pretreatment significantly increased CM viability but significantly decreased cardiac fibroblast viability. In rat neonatal CMs, cell death, as determined by lactate dehydrogenase (LDH) activity, was significantly reduced with hypoxia/NaNO2 pretreatment; and in hESC-CMs, hypoxia/NaNO2 pretreatment increased the BCL-2/BAX gene expression ratio, suggesting that hypoxia/NaNO2 pretreatment promotes cell viability by downregulating apoptosis. Additionally, we found a correlation between the prosurvival effect of hypoxia/NaNO2 pretreatment and the myoglobin content of the cells by comparing neonatal rat ventricular and atrial CMs, which express high and low myoglobin respectively. Functionally, hypoxia/NaNO2 pretreatment significantly improved the excitation threshold upon H/R injury to the level observed for uninjured cells, whereas pretreatment did not affect the maximum capture rate. Hence, hypoxia/NaNO2 pretreatment may serve as a strategy to increase CM survival in cardiac regenerative therapy applications and tissue engineering.

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Trans‐System Mechanisms Against Ischemic Myocardial Injury

Liu

Liang

Qin

et al. 2014

Comprehensive Physiology

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A mammalian organism possesses a hierarchy of naturally evolved protective mechanisms against ischemic myocardial injury at the molecular, cellular, and organ levels. These mechanisms comprise regional protective processes, including upregulation and secretion of paracrine cell-survival factors, inflammation, angiogenesis, fibrosis, and resident stem cell-based cardiomyocyte regeneration. There are also interactive protective processes between the injured heart, circulation, and selected remote organs, defined as trans-system protective mechanisms, including upregulation and secretion of endocrine cell-survival factors from the liver and adipose tissue as well as mobilization of bone marrow, splenic, and hepatic cells to the injury site to mediate myocardial protection and repair. The injured heart and activated remote organs exploit molecular and cellular processes, including signal transduction, gene expression, cell proliferation, differentiation, migration, mobilization, and/or extracellular matrix production, to establish protective mechanisms. Both regional and trans-system cardioprotective mechanisms are mediated by paracrine and endocrine messengers and act in coordination and synergy to maximize the protective effect, minimize myocardial infarction, and improve myocardial function, ensuring the survival and timely repair of the injured heart. The concept of the trans-system protective mechanisms may be generalized to other organ systems-injury in one organ may initiate regional as well as trans-system protective responses, thereby minimizing injury and ensuring the survival of the entire organism. Selected trans-system processes may serve as core protective mechanisms that can be exploited by selected organs in injury. These naturally evolved protective mechanisms are the foundation for developing protective strategies for myocardial infarction and injury-induced disorders in other organ systems.

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Ischemic Preconditioning in Isolated Cells

Cited by 48 publications

References 47 publications

Expression of constitutively stable hybrid hypoxia-inducible factor-1α protects cultured rat cardiomyocytes against simulated ischemia-reperfusion injury

Expression of constitutively stable hybrid hypoxia-inducible factor-1α protects cultured rat cardiomyocytes against simulated ischemia-reperfusion injury

Combined hypoxia and sodium nitrite pretreatment for cardiomyocyte protection in vitro

Trans‐System Mechanisms Against Ischemic Myocardial Injury

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