JNK1 is inactivated during thiamine deficiency-induced apoptosis in human neuroblastoma cells

Wang, James J.-L.; Hua, Zhaolin; Fentress, Hugh M.; Singleton, Charles K.

doi:10.1016/s0955-2863(00)00067-x

Cited by 21 publications

(11 citation statements)

References 41 publications

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“…Structural remodeling and the destruction of cardiomyocyte mitochondria were also observed with TD [20]. A similar finding was observed in a study with human neuroblastoma cells cultured under TD conditions [23]. …”

Section: Introductionsupporting

confidence: 71%

The effect of thiamine deficiency on inflammation, oxidative stress and cellular migration in an experimental model of sepsis

et al. 2014

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BackgroundSepsis is a prevalent condition in critically ill patients and may be associated with thiamine deficiency (TD). The aim of this study was to evaluate the effect of TD on inflammation, oxidative stress and cellular recruitment in a sepsis model.MethodsThe experimental sepsis model, cecal ligation and puncture (CLP), was utilized on mice in comparison with a sham procedure. The following four groups were compared against each other: SHAM with AIN93G complete chow, SHAM with thiamine deficient (TD) chow, CLP with AIN93G complete chow, and CLP with TD chow. Thiamine pyrophosphate (TPP) blood concentrations were determined, and blood and peritoneal fluid were evaluated for differences in TNF-alpha, IL-1, IL-6, KC and MCP-1/CCL2 levels. In addition, the levels of 4-HNE adducts in liver proteins were evaluated by Western Blot.ResultsThe mean TPP blood concentration from the mice fed with the complete chow was 303.3 ± 42.6 nmol/L, and TD occurred within 10 days. TNF-α and MCP-1 concentrations in the peritoneal fluid were significantly greater in the CLP with TD chow group when compared with the other groups. The blood IL-1β level, however, was lower in the CLP with TD chow group. Liver 4-HNE levels were highest in the TD chow groups. Blood mononuclear cell numbers, as well as peritoneal total leukocyte, mononuclear cell and neutrophil numbers were greater in the CLP with TD chow group. Peritoneal bacterial colony forming units (CFU) were significantly lower in the CLP with TD chow group.ConclusionTD was associated with greater bacterial clearance, oxidative stress and inflammatory response changes.

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Section: Introductionsupporting

confidence: 71%

The effect of thiamine deficiency on inflammation, oxidative stress and cellular migration in an experimental model of sepsis

et al. 2014

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“…TD can lead to activation of caspases. TD-induced stress may lead to the inactivation of C-Jun N-terminal kinase 1 (JNK1) and the loss of its cellular protective function from programmed cell death [53]. Recent results suggest that TD triggers apoptosis by activating caspase-3 mediated signaling pathway which leads to neuronal loss [15].…”

Section: Discussionmentioning

confidence: 99%

Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model

Karuppagounder

Shi

et al. 2009

Neurobiology of Aging

125

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Mitochondrial dysfunction, oxidative stress and reductions in thiamine-dependent enzymes have been implicated in multiple neurological disorders including Alzheimer's disease (AD). Experimental thiamine deficiency (TD) is an established model for reducing the activities of thiamine-dependent enzymes in brain. TD diminishes thiamine dependent enzymes throughout the brain, but produces a time-dependent selective neuronal loss, glial activation, inflammation, abnormalities in oxidative metabolism and clusters of degenerating neurites in only specific thalamic regions. The present studies tested how TD alters brain pathology in Tg19959 transgenic mice over expressing a double mutant form of the amyloid precursor protein (APP). TD exacerbated amyloid plaque pathology in transgenic mice and enlarged the area occupied by plaques in cortex, hippocampus and thalamus by 50%, 200% and 200%, respectively. TD increased Aβ 1-42 levels by about three-fold, β-CTF (C99) levels by 33% and β-secretase (BACE1) protein levels by 43%. TD induced inflammation in areas of plaque formation. Thus, the induction of mild impairment of oxidative metabolism, oxidative stress and inflammation induced by TD alters metabolism of APP and/or Aβ and promotes accumulation of plaques independent of neuron loss or neuritic clusters.

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“…However, in response to a physiological stress, which may depend on the particular cell type or organism, ThTP accumulates inside the cells where, possibly 1486 A. F. Makarchikov et al Thiamine triphosphate and thiamine triphosphatase through the phosphorylation of some target proteins, it may induce a reaction to stress, favoring cell survival. Indeed, at least in neuroblastoma cells, thiamine deficiency has recently been shown to result in cellular stress leading to the loss of JNK1 activity rendering the cells more sensitive to apoptosis [45]. During thiamine deficiency, ThTP might not be available anymore, contributing to cell death.…”

Section: Discussionmentioning

confidence: 99%

“…Thiamine is an ancient molecule, probably already present in the RNA world. Indeed, thiamine, like riboflavin and flavin mononucleotides, may directly interact with mRNA molecules for the control of gene expression at the level of transcription [45] or translation [46]. These completely new mechanisms emphasize our point of view that thiamine is far from having given away all its secrets.…”

Section: Discussionmentioning

confidence: 99%

Thiamine triphosphate and thiamine triphosphatase activities: from bacteria to mammals

Makarchikov

Lakaye

Gulyai

et al. 2003

Cellular and Molecular Life Sciences (CMLS)

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In most organisms, the main form of thiamine is the coenzyme thiamine diphosphate. Thiamine triphosphate (ThTP) is also found in low amounts in most vertebrate tissues and can phosphorylate certain proteins. Here we show that ThTP exists not only in vertebrates but is present in bacteria, fungi, plants and invertebrates. Unexpectedly, we found that in Escherichia coli as well as in Arabidopsis thaliana, ThTP was synthesized only under particular circumstances such as hypoxia (E. coli) or withering (A. thaliana). In mammalian tissues, ThTP concentrations are regulated by a specific thiamine triphosphatase that we have recently characterized. This enzyme was found only in mammals. In other organisms, ThTP can be hydrolyzed by unspecific phosphohydrolases. The occurrence of ThTP from prokaryotes to mammals suggests that it may have a basic role in cell metabolism or cell signaling. A decreased content may contribute to the symptoms observed during thiamine deficiency.

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JNK1 is inactivated during thiamine deficiency-induced apoptosis in human neuroblastoma cells

Cited by 21 publications

References 41 publications

The effect of thiamine deficiency on inflammation, oxidative stress and cellular migration in an experimental model of sepsis

The effect of thiamine deficiency on inflammation, oxidative stress and cellular migration in an experimental model of sepsis

Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse model

Thiamine triphosphate and thiamine triphosphatase activities: from bacteria to mammals

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