Regulation of energy metabolism by creatine in cardiac and skeletal muscle cells in culture

Seraydarian, Maria W.; Artaza, Luz

doi:10.1016/0022-2828(76)90009-2

Cited by 36 publications

(8 citation statements)

References 21 publications

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“…However, the capacity of PC biosynthesis is likely to differ among cell types. CR supplementation was found to increase the PC concentration in endothelial cells to 74 nmol mg protein À1 , which value was comparable to that in skeletal muscle cells (Seraydarian and Artaza, 1976). However, PC concentration in myocardial cells has been reported to be 107 nmol mg protein À1 after CR supplementation (Seraydarian and Artaza, 1976).…”

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confidence: 76%

“…Extracellular CR is tightly linked to intracellular energy pools in myocardial and skeletal muscle cells (Seraydarian and Artaza, 1976). On the other hand, we demonstrated that CR supplementation stimulates endothelial cells to generate intracellular PC by CR uptake through a CR transporter.…”

Section: Discussionmentioning

confidence: 99%

“…CR supplementation was found to increase the PC concentration in endothelial cells to 74 nmol mg protein À1 , which value was comparable to that in skeletal muscle cells (Seraydarian and Artaza, 1976). However, PC concentration in myocardial cells has been reported to be 107 nmol mg protein À1 after CR supplementation (Seraydarian and Artaza, 1976). In contrast with the level of PC, that of intracellular ATP was found to be unsusceptible to CR supplementation or a CR transporter antagonist.…”

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confidence: 84%

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Anti‐inflammatory activity of creatine supplementation in endothelial cells in vitro

Nomura

Zhang

Sakamoto

et al. 2003

British J Pharmacology

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1 Creatine (CR) supplementation augments muscle strength in skeletal muscle cells by increasing intracellular energy pools. However, the effect of CR supplementation on endothelial cells remains to be clarified. 2 In this study, we investigated whether CR supplementation had any anti-inflammatory activity against human pulmonary endothelial cells in culture.3 We confirmed that supplementation with 0.5 mm CR significantly increased both intracellular CR and phosphocreatine (PC) through a CR transporter while keeping intracellular ATP levels constant independent of CR supplementation and a CR transporter antagonist. 4 In the assay system of endothelial permeability, supplementation with 5 mm CR significantly suppressed the endothelial permeability induced by serotonin and H 2 O 2 . 5 In cell adhesion experiments, supplementation with 5 mm CR significantly suppressed neutrophil adhesion to endothelial cells. 6 In the measurement of adhesion molecules, CR supplementation with more than 0.5 mm CR significantly inhibited the expressions of ICAM-1 and E-selectin on endothelial cells, and the inhibition was significantly suppressed by an adenosine A 2A receptor antagonist. 7 The present study suggests that CR supplementation has anti-inflammatory activities against endothelial cells. British Journal of Pharmacology (2003) 139, 715 -720. doi:10.1038/sj.bjp.0705316 Keywords: Creatine;endothelial cell; H 2 O 2 ; permeability; phosphocreatine; ATP; serotonin; adhesion; ICAM-1; E-selectin Abbreviations: CR, creatine; Dil-Ac-LDL, LDL labeled with 1,1 0 -dioctadecyl-3,3,3 0 ,3 0 -tetramethylindo-carbocyanine perchlorate; EBM, endothelial cell basal medium; FITC-dex, fluorescein isothiocyanate-dextran; FMLP, n-formyl-MetLeu-Phe; GPA, b-guanidinopropionic acid; HBSS, Hank's balanced saline solution; LDL, low-density lipoprotein; b-NAD þ , b-nicotinamide adenine dinucleotide; PC, phosphocreatine IntroductionCreatine (CR) is tightly linked to the intracellular energy under the form of ATP (Wyss & Kaddurah-Daouk, 2000). Cells take in CR from the blood stream through a CR transporter and store it as CR and its phosphorylated form, phosphocreatine (PC) (Snow & Murphy, 2001). CR receives a phosphoryl group from ATP to generate PC by using the CR kinase inside cells. Intracellular ATP has such a short half-life that cells are equipped with two major channels of ATP supply. One is glycolysis and oxidative phosphorylation; the other is the PC energy system. While the former constantly provides ATP, the latter works on acute demand as an energy buffer to maintain an intracellular ATP level. Because PC transfers the phosphoryl group to ADP to synthesize ATP quickly, the total amount of ATP and PC represents an intracellular energy pool. The PC energy system is well characterized in the case of skeletal muscle cells because about 94% of CR is distributed therein (Wyss & Kaddurah-Daouk, 2000). It is known that supplementation with high-dose CR further increases intracellular energy pools of muscle tissue as well as serum CR levels in vivo. ...

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confidence: 76%

Section: Discussionmentioning

confidence: 99%

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confidence: 84%

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Anti‐inflammatory activity of creatine supplementation in endothelial cells in vitro

Nomura

Zhang

Sakamoto

et al. 2003

British J Pharmacology

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“…of mean, n = 12) after the onset of hypoxic superfusion. The results are shown in (Seraydarian & Artaza, 1976), we reasoned that inclusion of creatine in the incubation medium would increase molecular layer creatine phosphate. We have shown this is true for whole slices (Whittingham & Lipton, 1982).…”

Section: Methodsmentioning

confidence: 99%

Reduced ATP concentration as a basis for synaptic transmission failure during hypoxia in the in vitro guinea‐pig hippocampus

Lipton

Whittingham

1982

The Journal of Physiology

208

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SUMMARY1. Experiments were performed to determine whether a decrease in tissue ATP contributes to the rapid failure of cerebral synaptic transmission during hypoxia. Transmission between the perforant path and the dentate granule cells in the in vitro hippocampus was studied.2. Hippocampal slice ATP is decreased by -15% at the time that the evoked response begins to diminish in standard Krebs bicarbonate buffer. This is about 2 min after the onset of hypoxia.3. When transmission failure is accelerated by increasing extracellular K+ from 4-4 to 13-4 mM, the evoked response begins to decay about 30 see after exposure to hypoxia. There is no decrease in hippocampal slice ATP at this time. 4. However, ATP in the molecular layer (the synaptic region of the tissue) is decreased by -15 % at the time the evoked response begins to decay in the slices exposed to elevated K+ concentration. 5. Exposing the hippocampal slice to 25 mM-creatine for 3 hr elevates molecular layer phosphocreatine fourfold. Synaptic transmission during hypoxia survives three times as long as it does in the absence of creatine.6. In the creatine fortified medium, molecular layer ATP no longer declines within 30 sec of hypoxia. However the molecular layer ATP does decline within 90 sec of hypoxia, the time at which the evoked response begins to decay in this creatine-fortified buffer.7. The results establish that ATP in the region of the active synapses is lowered when the first signs of electrophysiological failure appear during hypoxia. They also show that maintaining ATP for longer than normal during hypoxia is associated with a prolonged maintenance of the evoked response. They thus suggest that a decline in ATP is one factor causing hypoxic block of synaptic transmission.8. It is further suggested that the very rapid failure of the electroencephalogram during anoxia may also result from a decline in ATP.

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“…This approach was based on experiments by Seraydarian and coworkers on cultured muscle tissue. 11 This manipulation greatly prolonged survival of the evoked response during anoxia (Fig. 1), while at the same time preventing the rapid fall in ATP that normally occurs.…”

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Cerebral Neuronal Transmission

Lipton¹,

Whittingham²

1981

Semin Respir Crit Care Med

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Low oxygen tension profoundly disturbs cerebral function. Studies in the 1930s demonstrated a rapid loss of EEG acitivity when animals breathed nitrogen. 2,14 The studies of Siesjo and many coworkers have described the steady-state effects of hypoxia on neural function and cerebral metabolites, particularly those involved in energy metabolism. 12 They highlight a central problem in our understanding of the effects of hypoxia by showing a clear neuronal dysfunction in the absence of any measured change in brain ATP concentrations. Thus, 30' exposures to levels of hypoxia which lead to a large slow-wave EEG pattern and in some cases EEG flattening 13 had no effect on cortical or brain stem ATP concentrations; 4,8 on the other hand, pH and phosphocreatine decreased. 1 Furthermore, neurotransmitter metabolism is compromised at the moderate levels of hypoxia that alter cerebral function. 3,5 These studies suggest that decreased ATP is not the cause of cerebral dysfunction in hypoxia. However, there are still reasons for considering the issue as an open one. While observed rates of monoamine and acetylcholine synthesis are depressed directly by hypoxia, 3 ' 5 there is no evidence that the release of neurotransmitter is compromised. Also, ATP measurements are made on whole cortices, which may not reflect concentrations in the sensitive synaptic regions of the brain.The acute effects of anoxia illustrate a similar dilemma in establishing the biochemical basis of cerebral dysfunction. Several groups of workers who have simultaneously measured EEG activity and metabolite changes have noted that EEG activity vanishes at a time when ATP concentration in brain or cortex is decreased by a very small percentage or not at all. 10 Again, while a fall in ATP may not cause the loss in EEG activity, the fact that ATP measurements are not confined to synaptic regions makes it impossible to interpret the results unequivocally.

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Regulation of energy metabolism by creatine in cardiac and skeletal muscle cells in culture

Cited by 36 publications

References 21 publications

Anti‐inflammatory activity of creatine supplementation in endothelial cells in vitro

Anti‐inflammatory activity of creatine supplementation in endothelial cells in vitro

Reduced ATP concentration as a basis for synaptic transmission failure during hypoxia in the in vitro guinea‐pig hippocampus

Cerebral Neuronal Transmission

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