Clofibrate-induced apoptosis is mediated by Ca2+-dependent caspase-12 activation

Matzno, Sumio; Yasuda, Shinya; Kitada, Yuka; Akiyoshi, Takeshi; Tanaka, Naoko; Juman, Sachiko; Shinozuka, Kazumasa; Nakabayashi, Toshikatsu; Matsuyama, Kenji

doi:10.1016/j.lfs.2005.08.003

Cited by 17 publications

(15 citation statements)

References 41 publications

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“…Our results suggest that this pathway is Ca 2+ related but μ-calpain independent, which results in caspase-12 activation. This is in agreement with the proposition of Matzno et al [19].…”

Section: Discussionsupporting

confidence: 94%

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Cardiotoxin III‐induced apoptosis is mediated by Ca²⁺‐dependent caspase‐12 activation in K562 cells

Yang

Chien

Chang

et al. 2008

J Biochem & Molecular Tox

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Cardiotoxin III (CTX III), a basic polypeptide with 60 amino acid residues isolated from Naja naja atra venom, has been reported to have anticancer activity. When K562 cells were treated with CTX III, cytosolic calcium concentration was rapidly and persistently increased. This CTX III-induced cell death was partially reversed by pretreatment with BAPTA/AM (20 microM), a chelator of intracellular Ca2+. Moreover, CTX III-induced apoptotic signals, such as caspase-12 and c-Jun N-terminal kinase (JNK) activation, were induced in a time-dependent manner and inhibited by BAPTA/AM. In contrast, the neutral protease micro-calpain, a key enzyme in endoplasmic reticulum (ER) stress-related apoptosis via caspase-12 activation, was unchanged during apoptosis. Taken together, our findings suggest CTX III-induced apoptosis is triggered by Ca2+ influx, then activated caspase-12 and JNK through micro-calpain-independent cascade, and consequently caused apoptosis.

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“…Our results suggest that this pathway is Ca 2+ related but μ-calpain independent, which results in caspase-12 activation. This is in agreement with the proposition of Matzno et al [19].…”

Section: Discussionsupporting

confidence: 94%

“…The latter always explains cytotoxic agent-induced effects in tumor cells [4,19]. Furthermore, new ER stress-induced apoptosis pathway, calcium-mediated caspase cascade has been given attention [17][18][19]. Intracellular calcium increment causes the activation of μ-calpain followed by caspase-12 activation.…”

Section: Discussionmentioning

confidence: 99%

Cardiotoxin III‐induced apoptosis is mediated by Ca²⁺‐dependent caspase‐12 activation in K562 cells

Yang

Chien

Chang

et al. 2008

J Biochem & Molecular Tox

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“…Recently, it was reported that clofibrate-induced myopathy is related to carcium influx (Ikemoto and Endo, 2001;Matzno et al, 2006). Hodel briefly reviewed clofibrate-induced 520 OKADA ET AL.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Susceptibility to Clofibrate Induction of Lesions in Rats

et al. 2007

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Morphological changes induced by clofibrate in type-1 predominant soleus, type-2 predominant tensor fasciae latae, and type-1 and -2 mixed biceps femoris muscles and diaphragm in rats were investigated. Administration of the agent at 500 or 750 mg/kg/day by oral gavage for 14 or 28 days caused lesions in the soleus muscle and diaphragm, bur no changes in the tensor fasciae latae and biceps femoris muscles. In soleus muscle, vacuolation of muscle fibers was observed in all animals treated with clofibrate, and degeneration of muscle fibers and infiltration of leukocytes were noted at 750 mg/kg/day. In diaphragm, vacuolation of muscle fibers was also observed in all animals treated with clofibrate, and these lesions were located in type-1 skeletal muscles densely stained with NADH-TR. The vacuoles seen in soleus muscle and diaphragm were positive for oil red O staining. In addition, increase of lipid droplets and mitochondrial hypertrophy was seen in soleus muscle, ultrastructurally. These data suggest that sensitivity to clofibrate-induced muscle toxicity differs among muscles, with type-1 fibers being susceptible.

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“…Caspase activities were assessed by cleavage of their specific substrates, as described previously. [16] Briefly, 24 h after drug treatment, the cells were washed twice with PBS and scraped. They were then harvested with 0.1% Triton X-100 and centrifuged at 4000g at 4 C for 10 min.…”

Section: Determination Of Caspase Activitiesmentioning

confidence: 99%

Synergistic action of statins and nitrogen-containing bisphosphonates in the development of rhabdomyolysis in L6 rat skeletal myoblasts

et al. 2009

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Objectives Nitrogen-containing bisphosphonates, which are widely used to treat osteoporosis, act as inhibitors of farnesyl pyrophosphate synthase, one of the key enzymes of the mevalonate pathway, and thus may have the potential to enhance the effect of statins (inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase). In this study, we evaluated the synergistic effect of two nitrogen-containing bisphosphonates, alendronate and risedronate, in statin-induced apoptosis in rat skeletal L6 myoblasts. Methods L6 rat myoblasts were differentiated with drugs. DNA fragmentation was measured and small GTPase was detected by immunoblotting. Key findings Alendronate and risedronate caused dose-dependent apoptosis of L6 myoblasts. Risedronate induced detachment of rho GTPase from the cell membrane, followed by activation of the caspase-8-related cascade. Risedronate-induced apoptosis was synergistically enhanced with atorvastatin and significantly reduced by addition of geranylgeraniol. By contrast, alendronate did not reduce membrane GTPases and the apoptosis was caspase independent. Conclusions These results suggest that risedronate-induced apoptosis is related to geranylgeranyl pyrophosphate depletion followed by rho detachment, whereas alendronate affects are independent of rho. Our results suggest a risk of synergistic action between nitrogen-containing bisphosphonates and statins in the development of rhabdomyolysis when treating osteoporosis in women with hyperlipidaemia.Statin-bisphosphonate synergism in rat myoblasts Sumio Matzno et al.

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Clofibrate-induced apoptosis is mediated by Ca2+-dependent caspase-12 activation

Cited by 17 publications

References 41 publications

Cardiotoxin III‐induced apoptosis is mediated by Ca²⁺‐dependent caspase‐12 activation in K562 cells

Cardiotoxin III‐induced apoptosis is mediated by Ca²⁺‐dependent caspase‐12 activation in K562 cells

Skeletal Muscle Susceptibility to Clofibrate Induction of Lesions in Rats

Synergistic action of statins and nitrogen-containing bisphosphonates in the development of rhabdomyolysis in L6 rat skeletal myoblasts

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Clofibrate-induced apoptosis is mediated by Ca2+-dependent caspase-12 activation

Cited by 17 publications

References 41 publications

Cardiotoxin III‐induced apoptosis is mediated by Ca2+‐dependent caspase‐12 activation in K562 cells

Cardiotoxin III‐induced apoptosis is mediated by Ca2+‐dependent caspase‐12 activation in K562 cells

Skeletal Muscle Susceptibility to Clofibrate Induction of Lesions in Rats

Synergistic action of statins and nitrogen-containing bisphosphonates in the development of rhabdomyolysis in L6 rat skeletal myoblasts

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Product

Resources

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Cardiotoxin III‐induced apoptosis is mediated by Ca²⁺‐dependent caspase‐12 activation in K562 cells

Cardiotoxin III‐induced apoptosis is mediated by Ca²⁺‐dependent caspase‐12 activation in K562 cells