Effects on mitochondrial metabolism of CCA, one inducer of neuroblastoma differentiation

Vayssière, Jean-Luc; Larcher, Jean-Christophe; Berthelot, Francis; Benlot, C.; Gros, François; Croizat, Bernard

doi:10.1016/0006-291x(86)90703-5

Cited by 9 publications

(4 citation statements)

References 12 publications

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“…Western blot anticytochrome c. To test for the presence of cytochrome c in the cytosol of infected cells, an adaptation to the method originally described by Vayssiére et al [29] to obtain mitochondria-free cytosol was used. Briefly, cells were harvested in the minimal possible volume of mitochondria isolation buffer (0.25 M sucrose, 0.5 mM ethylenediaminetetraacetic acid (EDTA)-K þ 10 mM Tris-HCl, 2 mg/ml of aprotinin, 10 mg/ml of leupeptin, 5 mg/ml of sodium orthovanadate, pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

Mycobacterium tuberculosis Virulence Correlates with Mitochondrial Cytochrome c Release in Infected Macrophages

et al. 2003

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Mitochondria are at the centre of molecular events involved in energy production, cell survival and apoptosis. Mitochondrial membrane potential (Dc m ) is maintained by cellular catabolic reactions and the electron transport chain of which cytochrome c is a constituent, whereas the proton leak pathway, ATP synthesis and turnover consume it. Mitochondrial alterations such as a drop in Dc m , swelling and cytochrome c release have been observed in apoptosis. However, there is a paucity of information concerning mitochondrial function in the course of intracellular infections, a process that must certainly induce stress on the host cell. This work analyses the effect that two strains of mycobacteria of opposing virulence have on the mitochondria of murine macrophages in the early stages of infection. It was found that infection of J774 cells with both Mycobacterium tuberculosis H37Ra and M. tuberculosis H37Rv readily induced changes in Dc m as well as in mitochondrial morphology at the ultrastructural level. In addition, an increase in cytosolic ATP was found at 24 h post infection with both strains of M. tuberculosis. Interestingly, only M. tuberculosis H37Rv was able to induce cytochrome c release from mitochondria to the cytosol, thus suggesting the occurrence in M. tuberculosis H37Rv of a specific factor(s) capable of regulating cytochrome c translocation. The precise role of cytochrome c release in the context of a mycobacterial infection remains to be elucidated.

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Section: Methodsmentioning

confidence: 99%

Mycobacterium tuberculosis Virulence Correlates with Mitochondrial Cytochrome c Release in Infected Macrophages

et al. 2003

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“…Cells were grown at 330C and shifted to 39.50C for various periods of times. They were then harvested, and 02 uptake was measured in fresh culture medium (11). Measurements were performed at 330C, since preliminary studies had shown that similar results are obtained at 330C or 39.50C (data not shown).…”

Section: Methodsmentioning

confidence: 99%

“…Boy, Reims, France) in the presence of emetine (100 pg/ml; Sigma), an inhibitor of cytoplasmic protein synthesis, and they were then labeled with [35S]methionine (37 TBq/mmol) at a concentration of 1.67 MBq/ml and incubated for 2 hr prior to harvesting. Cells were washed and harvested, and mitochondria were purified as described (11). Samples of mitochondrial proteins were run on SDS/polyacrylamide gels containing 15% acrylamide and 0.2% methylenebisacrylamide.…”

Section: Methodsmentioning

confidence: 99%

Commitment to apoptosis is associated with changes in mitochondrial biogenesis and activity in cell lines conditionally immortalized with simian virus 40.

Vayssière

Petit

Risler

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

288

150

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Rodent embryo cells immortalized with temperature-sensitive mutants of simian virus 40 large tumor (T) antigen have a proliferative potential that depends on temperature. At the restrictive temperature, heat-inactivation oflarge T antigen causes p53 release, growth arrest, and cell death.Morphological and molecular analysis indicate that the induced cell death corresponds to apoptosis. Flow cytometric analysis using a combination of forward light scatter and side scatter allows a discrimination of cells committed to apoptosis within the whole population. These cells display a reduction in cell size and a higher cellular density, confirming the apoptotic nature of the cell death. When cells exhibiting the morphological features of apoptosis were stained with a fluorescent probe of the mitochondrial membrane potential, a decreased accumulation of the dye was recorded. Measures of cellular respiration, performed with whole-cell populations, showed that the lower mitochondrial membrane potential (At,) correlates, as expected, with an uncoupling of electron transport from ATP production and is linked to the induction of apoptosis. We also show that this decrease in A'I is associated with a decrease in the rate ofmitochondrial translation. These events are detected at early stages of the apoptotic process, when most of the cells are not irreversibly committed to death, suggesting that mitochondria could be a primary target during apoptosis.Mammalian cells grown in culture exhibit a finite life-span for proliferation. After a variable number of divisions they stop dividing, undergo a variety of changes, and finally die. Some oncogenes have the ability to confer an unlimited proliferative potential (immortality) to primary cells in culture. In the case of polyomavirus-induced immortalization of rodent embryo fibroblasts, it has been shown that the unlimited proliferative capacity is maintained by the large tumor (T) antigen (1)(2)(3)(4) MATERIALS AND METHODSCell Lines and Cell Culture. The REtsAF and RELPB cell lines were isolated at low cell density from a rat embryo fibroblast culture infected with SV40 (2). REtsAF was obtained by using a temperature-sensitive tsA58 mutant and is temperature sensitive for immortalization, whereas RELPB was obtained with wild-type SV40 and is immortal at both 330 and 39.50C. REtsAF-Revl was derived from REtsAF by selection for proliferation at 39.50C (8

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“…Oxygen uptake was measured polarographically in a 2-ml cell at 37°C as described by Vayssière et al (1986) . For each experiment, ~10-20 X 10 6 cells ( suspended in their respective medium) were used and the OZ consumption in the presence of 1 mM NaCN was subtracted.…”

Section: Binding Of [3h] Pk 11195mentioning

confidence: 99%

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Bettendorff

Goessens

Sluse

1997

Molecular and Cellular Biochemistry

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Culture of neuroblastoma cells in the presence of low thiamine concentration (16 nM) and of the transport inhibitor amprolium leads to the appearance of signs of necrosis: the chromatin condenses, the oxygen consumption decreases and is uncoupled, the mitochondrial cristae are disorganized, the thiamine diphosphate-dependent dehydrogenase activities are impaired. When 10 microM thiamine are added to these cells, the basal respiration increases, the coupled respiration is restored and mitochondrial morphology is recovered within 1 h. Addition of succinate, which is oxidized via a thiamine diphosphate-independent dehydrogenase, to digitonin-permeabilized cells immediately restores a coupled respiration. Our results suggest that the slowing of the citric acid cycle is the cause of the biochemical lesion induced by severe thiamine deficiency and that part of the mitochondria remain functional.

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Effects on mitochondrial metabolism of CCA, one inducer of neuroblastoma differentiation

Cited by 9 publications

References 12 publications

Mycobacterium tuberculosis Virulence Correlates with Mitochondrial Cytochrome c Release in Infected Macrophages

Mycobacterium tuberculosis Virulence Correlates with Mitochondrial Cytochrome c Release in Infected Macrophages

Commitment to apoptosis is associated with changes in mitochondrial biogenesis and activity in cell lines conditionally immortalized with simian virus 40.

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