Inhibition of tumor necrosis factor‐induced apoptosis in transgenic mouse liver expressing creatine kinase

Hatano, Etsuro; Kanazawa, Akiyoshi; Tsuyuki, Shigeru; Shoji, Takuhito; Iwata, Satoru; Takahashi, Rei; Chance, Britton; Yamaoka, Yoshio

doi:10.1111/j.1478-3231.2004.0939.x

Cited by 30 publications

(12 citation statements)

References 49 publications

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“…The enzyme described as ''Macro CK'' [26,27] in previous reports has in fact been identified as ubiquitous MtCK, and a correlation between serum ubiquitous MtCK level and the pathological condition of nephrotoxicity in HIV patients receiving tenofovir has been reported [28]. Although the role of CK expression in the pathological liver has not been fully elucidated, CK expression in the liver of transgenic mice reportedly provokes tolerance against tumor necrosis factor-a-induced apoptosis [29], protection against hypoxia or endotoxin perfusion [30][31][32], and inhibition of pro-apoptotic mechanisms [33], suggesting a beneficial role of CK expression in the liver. In the current study, serum activity of MtCK was significantly higher in patients with cirrhosis and HCC caused by HBV or HCV virus than in subjects with no liver diseases.…”

Section: Discussionmentioning

confidence: 95%

Increased activity of serum mitochondrial isoenzyme of creatine kinase in hepatocellular carcinoma patients predominantly with recurrence

Soroida

Ohkawa

Nakagawa

et al. 2012

Journal of Hepatology

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Section: Discussionmentioning

confidence: 95%

Increased activity of serum mitochondrial isoenzyme of creatine kinase in hepatocellular carcinoma patients predominantly with recurrence

Soroida

Ohkawa

Nakagawa

et al. 2012

Journal of Hepatology

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“…Apoptosis was also induced in cultured human retinal pigment epithelial cells by incubating with cystine [53]. In addition, supplementation of creatine, a potent antioxidant [54], to the diet of mice fully prevents the apoptosis induced by TNF-a [55]. However, it must be emphasized that in cystinosis the cystine accumulated is synthesized in the lysosomes, and is not transported from the cytosol as is the case in the CDME model of cystinosis.…”

Section: Discussionmentioning

confidence: 95%

Antioxidant Effect of Cysteamine in Brain Cortex of Young Rats

et al. 2007

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Cysteamine is a cystine-depleting drug used in the treatment of cystinosis, a metabolic disorder caused by deficiency of the lysosomal cystine carrier. As a result, cystine accumulates within lysosomes in many tissues and organs, including the nervous system. Studies with cystine dimethyl ester loaded cells suggest that cystine might induce apoptosis through oxidative stress. Our objective was to investigate the effects of co-administration of cysteamine with the oxidant cystine dimethyl ester on several parameters of oxidative stress in the brain cortex of rats. Animals were injected with 1.6 micromol/g cystine dimethyl ester and/or 0.26 micromol/g body weight cysteamine. Cystine dimethyl ester induced lipoperoxidation, protein carbonylation, and stimulated superoxide dismutase, glutathione peroxidase and catalase activities, probably through the formation of free radicals. Cysteamine prevented those effects, possibly increasing cellular thiol pool and acting as a scavenger of free radicals. These results suggest that the antioxidant effect of cysteamine may be important in the treatment of cystinosis.

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“…Apoptosis was also induced in cultured human retinal pigment epithelial cells by incubating with cystine [47]. In addition, supplementation of creatine, a potent antioxidant [48], to the diet of mice fully prevents the apoptosis induced by tumor necrosis factor (TNF)α [49]. On the other hand, in other genetic (tyrosinemia, galactosemia, cytochrome C oxidase deficiency) and acquired (heavy metals, drugs, maleate) causes of Fanconi syndrome, the accumulated toxic substances cause energy deficit and oxidative stress [50].…”

Section: Discussionmentioning

confidence: 99%

Promotion of oxidative stress in kidney of rats loaded with cystine dimethyl ester

et al. 2007

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Cystinosis is a systemic genetic disease caused by a lysosomal transport deficiency accumulating cystine in most tissues. Although tissue damage might depend on cystine accumulation, the mechanisms of tissue damage are not fully understood. Studies performed in fibroblasts of cystinotic patients and in kidney cells loaded with cystine dimethyl ester (CDME) suggest that apoptosis is enhanced in this disease. Considering that oxidative stress is a known apoptosis inducer, our main objective was to investigate the effects of CDME loading on several parameters of oxidative stress in the kidney of young rats. Animals were injected twice a day with 1.6 micromol/g body weight CDME and/or 0.26 micromol/g body weight cysteamine (CSH) from the 16th to the 20th postpartum day and killed after 1 or 12 h. CDME induced lipoperoxidation and protein carbonylation and stimulated superoxide dismutase, glutathione peroxidase (GPx), and catalase activities, probably through the formation of superoxide anions, hydrogen peroxide, and hydroxyl free radicals. Coadministration of CSH, the drug used to treat cystinotic patients, prevented, at least in part, those effects, possibly acting as a scavenger of free radicals. These results suggest that the induction of oxidative stress might be one of the mechanisms leading to tissue damage in cystinotic patients.

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Inhibition of tumor necrosis factor‐induced apoptosis in transgenic mouse liver expressing creatine kinase

Abstract: The results indicate that TNFalpha-induced apoptosis was inhibited in CK transgenic mice livers by maintaining mitochondrial function.

Cited by 30 publications

References 49 publications

Increased activity of serum mitochondrial isoenzyme of creatine kinase in hepatocellular carcinoma patients predominantly with recurrence

Increased activity of serum mitochondrial isoenzyme of creatine kinase in hepatocellular carcinoma patients predominantly with recurrence

Antioxidant Effect of Cysteamine in Brain Cortex of Young Rats

Promotion of oxidative stress in kidney of rats loaded with cystine dimethyl ester

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