Thiamine deficiency in cardiac cells in culture

Zangen, A.; Shainberg, Asher

doi:10.1016/s0006-2952(97)00178-0

Cited by 32 publications

(15 citation statements)

References 29 publications

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“…The chamber was placed on the stage of an inverted phase contrast microscope (Olympus, Tokyo, Japan). Measurement of the contractions of the cardiomyocytes at baseline and in response to interventions was conducted using a video motion detector system as described in detail by Zangen and Shainberg (1997). Analog tracing was recorded using an oscilloscope joined through a specially designed interface to an IBM computer, and kinetic data were analyzed by the Microsoft Excel program.…”

Section: Tpen Protects Cardiocytes By Preserving Ca 2؉ Homeostasismentioning

confidence: 99%

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N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca²+ Homeostasis

Shmist¹,

Kamburg²,

Ophir³

et al. 2005

J Pharmacol Exp Ther

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N,N,NЈ,NЈ-Tetrakis(2-pyridylmethyl)-ethylenediamine (TPEN), a transition-metal chelator, was recently found to protect against myocardial ischemia-reperfusion injury. The goals of this study were to investigate the in vivo antiarrhythmic and antifibrillatory potential of TPEN in rats and guinea pigs and to study the in vitro effects of TPEN on calcium homeostasis in cultured newborn rat cardiac cells in normoxia and hypoxia. We demonstrated on an in vivo rat model of ischemia-reperfusion that TPEN abolishes ventricular fibrillation incidence and mortality and decreases the incidence and duration of ventricular tachycardia. To elucidate the mechanism of cardioprotection by TPEN, contraction, synchronization, and intracellular calcium level were examined in vitro. We have shown for the first time that TPEN prevented the increase in intracellular Ca 2ϩ levels (

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Section: Tpen Protects Cardiocytes By Preserving Ca 2؉ Homeostasismentioning

confidence: 99%

“…The cellular contraction activity of cultured cardiomyocytes was analyzed by a video technique previously described (Zangen and Shainberg, 1997;Shneyvays et al, 1998). The majority of the cultured cells exhibited synchronized spontaneous contractions (Fig.…”

Section: Tpen Protects Cardiomyocytes From Necrosis and Decrease Of Mmentioning

confidence: 99%

N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca²+ Homeostasis

Shmist¹,

Kamburg²,

Ophir³

et al. 2005

J Pharmacol Exp Ther

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“…Thiamine pyrophosphate is an important cofactor in several vital enzymatic reactions involved in metabolism and energy production (34,39). Following its uptake by the cell, thiamine rapidly undergoes pyrophosphorylation, yielding thiamine pyrophosphate, which is the active substance.…”

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confidence: 99%

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Oliveira¹,

Guatimosim²,

Castro³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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tensive work has been done regarding the impact of thiamine deprivation on the nervous system. In cardiac tissue, chronic thiamine deficiency is described to cause changes in the myocardium that can be associated with arrhythmias. However, compared with the brain, very little is known about the effects of thiamine deficiency on the heart. Thus this study was undertaken to explore whether thiamine deprivation has a role in cardiac arrhythmogenesis. We examined hearts isolated from thiamine-deprived and control rats. We measured heart rate, diastolic and systolic tension, and contraction and relaxation rates. Whole cell voltage clamp was performed in rat isolated cardiac myocytes to measure L-type Ca 2ϩ current. In addition, we investigated the global intracellular calcium transients by using confocal microscopy in the line-scan mode. The hearts from thiaminedeficient rats did not degenerate into ventricular fibrillation during 30 min of reperfusion after 15 min of coronary occlusion. The antiarrhythmogenic effects were characterized by the arrhythmia severity index. Our results suggest that hearts from thiamine-deficient rats did not experience irreversible arrhythmias. There was no change in L-type Ca 2ϩ current density. Inactivation kinetics of this current in Ca 2ϩ -buffered cells was retarded in thiamine-deficient cardiac myocytes. The global Ca 2ϩ release was significantly reduced in thiaminedeficient cardiac myocytes. The amplitude of caffeine-releasable Ca 2ϩ was lower in thiamine-deficient myocytes. In summary, we have found that thiamine deprivation attenuates the incidence and severity of postischemic arrhythmias, possibly through a mechanism involving a decrease in global Ca 2ϩ release.arrhythmia; calcium current; confocal microscopy THIAMINE DEFICIENCY CAUSES cardiovascular and neurological damage that presents clinically as beriberi. Thiamine pyrophosphate is an important cofactor in several vital enzymatic reactions involved in metabolism and energy production (34, 39). Following its uptake by the cell, thiamine rapidly undergoes pyrophosphorylation, yielding thiamine pyrophosphate, which is the active substance. Extensive work has been done regarding the impact of thiamine deprivation on the nervous system. However, very little is known about the effects of thiamine deficiency on the myocardium (5). Cappelli et al. (5) have shown evidence that supports the view that cardiac contractility is deeply affected in the rat by thiamine deficiency. Thiamine is also considered a clinically important factor in heart function, and its deficiency has been reported to cause heart failure (28, 33, 35). The general view that reperfusion of the ischemic myocardium exerts a beneficial effect by preventing the ischemiainduced changes in cardiac performance has been supported by a number of studies; however, reperfusion after a certain critical time has been shown to be deleterious to cardiac function (16). Intracellular Ca 2ϩ has an important role in heart function, and studies have been conducted to investigate pos...

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“…0.3-0.5 ng/mg protein) were similar to the levels determined in the other cells. 15 These initial results obtained in B lymphocytes may suggest that the level of the phosphorylated form of thiamine is not a feature of the neurodegeneration phenotype. Bettendorff et al obtained similar results in brains of patient with frontal lobe degeneration of the non-Alzheimer's type.…”

Section: Discussionmentioning

confidence: 98%

“…The method was based on monitoring the decrease of substrate k-Ile (keto-isoleucine sodium salt (k-Ile), 3 mM, Sigma Aldrich) content in the time monitored by specific colorimetric reaction with DNPH (2,4-dinitrophenylhydrazine, POCH) at 450 nm. 15 The absorbance rate was corrected by a respective blank substraction (reaction performed as above). BCKDHC specific activity was calculated with regard to calibration curve prepared from k-Ile solution in a range of 1.5-3.0 mM and expressed in nmol/(min × mg protein).…”

Section: Bckdhc Activity Assaymentioning

confidence: 99%

Role of thiamine in Huntington’s disease pathogenesis: In vitro studies

Gruber-Bzura¹,

Krzysztoń-Russjan²,

Bubko³

et al. 2017

Adv Clin Exp Med

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Thiamine deficiency in cardiac cells in culture

Cited by 32 publications

References 29 publications

N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca²+ Homeostasis

N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca²+ Homeostasis

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Role of thiamine in Huntington’s disease pathogenesis: In vitro studies

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Thiamine deficiency in cardiac cells in culture

Cited by 32 publications

References 29 publications

N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca2+ Homeostasis

N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca2+ Homeostasis

Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Role of thiamine in Huntington’s disease pathogenesis: In vitro studies

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N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca²+ Homeostasis

N,N,N′,N′-Tetrakis(2-pyridylmethyl)-ethylenediamine Improves Myocardial Protection against Ischemia by Modulation of Intracellular Ca²+ Homeostasis