Apoptosome formation and caspase activation: is it different in the heart?

Czerski, Lech; Núñez, Gabriel

doi:10.1016/j.yjmcc.2004.04.016

Cited by 66 publications

(47 citation statements)

References 122 publications

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“…Hence, we studied the mechanism of apoptosis induction in OSCC cells in response to DAM and NDAM in vitro. Apoptosis is one of the most important objectives for cancer therapy including chemotherapy and chemoprevention (Czerski and Nuñez 2004). Apoptosis is characterized by particular morphological as well as biochemical alterations, which include cell shrinkage, nuclear condensation and fragmentation, plasma membrane blebbing, formation of apoptotic bodies in addition to loss of cell contacts to neighbor cells (Nishida et al 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Statistically significant differences between control and treated cells were set at **P \ 0.01 Cytochrome c is an essential mediator of programmed cell death through the intrinsic pathway. Apoptotic stimulus triggers the release of Cytochrome c from the mitochondria into the cytosol (Czerski and Nuñez 2004). In the present study, there was a significant increase in the concentration of Cytochrome c in DAM Caspase-3/7 7.4 9 10 4 ± 2.9 9 10 Caspase-8 9.5 9 10 3 ± 3.2 9 10 9.9 9 10 3 ± 7.5 9 10 9.8 9 10 3 ± 5.6 9 10 9.8 9 10 (Table 7; Figs.…”

Section: Flow Cytometric Analysis Of Apoptosis By Fitcannexin V/pimentioning

confidence: 99%

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Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

et al. 2016

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Oral cancer is the eleventh most prevalent cancer worldwide. The most prevalent oral cancer is oral squamous cell carcinoma (OSCC). Damnacanthal (DAM) and nordamnacanthal (NDAM), the anthraquinone compounds, are isolated from the root of Morinda citrifolia L. (Noni), which has been used for the treatment of several chronic diseases including cancer. The objectives of this study were to evaluate the cytotoxicity, cell death mode, cell cycle, and the molecular mechanism of apoptosis induced by DAM and NDAM on OSCC. The cytotoxic effects of these compounds against OSCC cell lines were determined by MTT assay. The cell death mode was analysed by DNA laddering and FITC-annexin V/PI flow cytometric assays. In addition, the mechanism of apoptosis induced by DAM and NDAM was detected using mitochondrial membrane potential, Cytochrome c, and caspases assays. Finally, the effect of DAM and NDAM on cell cycle phase distribution of OSCC cells was detected by flow cytometry. In the present study, DAM and NDAM showed cytotoxicity towards OSCC cell lines and the maximum growth inhibition for both compounds was observed in H400 cells with IC 50 value of 1.9 and 6.8 lg/ml, respectively, after 72 h treatment. The results also demonstrated the inhibition of H400 OSCC cells proliferation, internucleosomal cleavage of DNA, activation of intrinsic apoptosis pathway, and cell cycle arrest caused by DAM and NDAM. Therefore, these findings suggest that DAM and NDAM can be potentially used as antitumor agents for oral cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Flow Cytometric Analysis Of Apoptosis By Fitcannexin V/pimentioning

confidence: 99%

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

et al. 2016

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“…Mitochondria play crucial roles by the apoptotic proteins, such as cytochrome c (Green et al, 1998;Jeong et al, 2008;Spierings et al, 2005). Previous studies have shown that cytochrome c has two main functions, that is, it controls cellular metabolism and apoptosis and activates the caspase cascade (Budihardjo et al, 1999;Cai et al, 1998;Czerski & Nuñez, 2004;Simonian et al, 1997). The caspases are a family of proteins that belong to a group of enzymes called cysteine proteases and caspases, and are major executors of apoptotic processes (Earnshaw et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Schizandra chinensisextracts induce apoptosis in human gastric cancer cells via JNK/p38 MAPK activation and the ROS-mediated/mitochondria-dependent pathway

Kim

Lee

Park

et al. 2014

Pharmaceutical Biology

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Objectives: This study investigates the mechanism of SCE-induced apoptosis in AGS human gastric cancer cells. Materials and methods: SCE concentrations from 100 to 400 mg/ml were used. Cell viabilities were determined using MTT assay. Members of the Bcl-2 family and Bax were detected by Western blotting. RT-PCR was performed to measure the expression level of the Fas/FasL pro-apoptotic genes.Results: SCE inhibited the proliferation AGS cells for 24 or 72 h (inhibition by 3.1% ± 5.2% at 100 mg/ml and 87.3% ± 7.6% at 400 mg/ml at 24 h and by 40.2% ± 5.3% 100 mg/ml and 95.3% ± 1.3% 400 mg/ml at 72 h) and increased the sub-G1 phase (25.3% ± 5.2% at 100 mg/ml and 370.2% ± 7.2% at 400 mg/ml) and the mitochondrial membrane depolarization (11.2% ± 2.1% at 100 mg/ml and 311.5% ± 6.1% at 400 mg/ml). The SCE-induced apoptotic cell death showed the down-regulation of Bcl-2, but up-regulation of Bax. Subsequently, SCE increased the expression level of Fas/FasL, activated caspase-9 and -3, and increased reactive oxygen species generation. Also, JNK II inhibitor or a p38 MAPK inhibitor inhibited SCE-induced cell death. Discussion and conclusion: These results indicate that SCE might be an effective chemotherapeutic for the treatment of human gastric cancer.

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“…In vitro, the cell releases predisposing factors in conjunction with the cell membrane receptor via aggregation to become a composite body (Czerski and Nuñez 2004). The FASL/FAS/TNF-α pathway incorporates adaptive proteins such as the Fas-associated death domain (FADD), which uses the death domain (DD) to bind death receptors, such as the pro-caspase-8 or procaspase-10 interaction platform to activate caspase-8 or caspase-10 molecules, respectively, that activate other proteins in the downstream signaling pathway (Bishopric et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

Lai

Kuo³

et al. 2014

AGE

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Cardiovascular disease is the second leading cause of death (9.1 %) in Taiwan. Heart function deteriorates with age at a rate of 1 % per year. As society ages, we must study the serious problem of cardiovascular disease. SIRT1 regulates important cellular processes, including anti-apoptosis, neuronal protection, cellular senescence, aging, and longevity. In our previous studies, rats with obesity, high blood pressure, and diabetes exhibiting slowed myocardial performance and induced cell apoptosis were reversed via sports training AGE (2014) 36:9706

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Apoptosome formation and caspase activation: is it different in the heart?

Cited by 66 publications

References 122 publications

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

Cell cycle arrest and mechanism of apoptosis induction in H400 oral cancer cells in response to Damnacanthal and Nordamnacanthal isolated from Morinda citrifolia

Schizandra chinensisextracts induce apoptosis in human gastric cancer cells via JNK/p38 MAPK activation and the ROS-mediated/mitochondria-dependent pathway

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

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