Mitochondrial outer-membrane permeabilization and remodelling in apoptosis

Jourdain, Alexis A.; Martinou, Jean‐Claude

doi:10.1016/j.biocel.2009.05.001

Cited by 108 publications

(78 citation statements)

References 98 publications

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“…Total Bak is bound to the outer mitochondrial membrane (16) and is activated upon homodimerization induced by the same stimuli as Bax (34). …”

Section: Discussionmentioning

confidence: 99%

“…We could demonstrate cytosolic distribution of cytochrome c in both CBMO and PBMO (Figure 5). However, Jourdain et al (34) suggested that only total release of cytochrome c leads to apoptosis, while a partial release might not be sufficient for caspase activation. We therefore speculate that cytochrome c release might be hampered in CBMO, possibly because of antiapoptotic distribution of Bcl-2 proteins, while in PBMO, the amount of released cytochrome c may be sufficient for apoptosis induction.…”

Section: Articlesmentioning

confidence: 99%

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Neonatal monocytes express antiapoptotic pattern of Bcl-2 proteins and show diminished apoptosis upon infection with Escherichia coli

et al. 2014

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Background:Neonates show sustained inflammation after a bacterial infection, which is associated with inflammatory diseases like bronchopulmonary dysplasia or periventricular leucomalacia. Physiologically, inflammation is terminated early after the removal of the invading pathogens by phagocytosisinduced cell death (PICD) of immune effector cells. Earlier results showed reduced PICD in neonatal monocytes. The underlying molecular mechanisms are unknown. We hypothesize that the reduced PICD in neonatal monocytes is regulated through the proteins of the B-cell lymphoma 2 (Bcl-2) protein family. Methods: mRNA and protein expression of Bcl-2 family proteins in cord blood and adult peripheral blood monocytes infected with Escherichia coli were analyzed by quantitative real-time PCR and flow cytometry and cytochrome c release by fluorescence microscopy. results: mRNA expression of antiapopototic Bcl-xL was upregulated in cord blood monocytes (CBMO), whereas proapoptotic Bim tended to be higher in peripheral blood monocytes (PBMO). Upon infection, Bax was more strongly expressed in PBMO compared with CBMO. The pro/antiapoptotic balance was skewed toward survival in CBMO and apoptosis in PBMO. Cytochome c release into the cytosol was enhanced in PBMO compared with CBMO. conclusion: Bcl-2 proteins are involved in reduced PICD in neonatal monocytes. These findings are another step toward the understanding of sustained inflammation in neonates.

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“…Total Bak is bound to the outer mitochondrial membrane (16) and is activated upon homodimerization induced by the same stimuli as Bax (34). …”

Section: Discussionmentioning

confidence: 99%

Section: Articlesmentioning

confidence: 99%

Neonatal monocytes express antiapoptotic pattern of Bcl-2 proteins and show diminished apoptosis upon infection with Escherichia coli

et al. 2014

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“…Both pathways can eventually lead to the activation of caspases and nucleases, resulting in cell apoptosis. Mitochondrial outer membrane permeabilization (MOMP), a key commitment step in the induction of cellular apoptosis, is often required for activation of the caspase proteases (26,27). It is important that the electrochemical gradient across the mitochondrial membrane collapses during the process of MOMP (28).…”

Section: Discussionmentioning

confidence: 99%

Millimeter wave radiation induces apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 human chondrosarcoma cells

Ye²,

Cai³

et al. 2011

Oncol Rep

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Abstract. The efficacy and safety of millimeter wave radiation has been proven for various types of malignant tumors. However, the mechanisms underlying effects of millimeter wave radiation on apoptosis are still unclear. The present study was undertaken to examine the effects of millimeter wave radiation on cell apoptosis and mitochondrial membrane potential, and to determine the molecular mechanism of millimeter wave radiation-induced apoptosis by investigating the expression of Bcl-2 family proteins (Bcl-2, Bax), caspase-9 and caspase-3 in SW1353 cells. We found that millimeter wave radiation suppressed the viability of SW1353 cells, demonstrating that millimeter wave radiation induced cell apoptosis and reduced cell viability in a time-dependent manner. Furthermore, we observed that treatment of cells with millimeter wave radiation significantly induced loss of mitochondrial membrane potential, upregulated proapoptotic Bax, caspase-9 and caspase-3, but did not significantly change levels of antiapoptotic Bcl-2. These data suggested that millimeter wave radiation may induce apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 cells.

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“…Indeed, the presence of cardiolipin in mitochondria plays a functional role in protein interactions (Cosentino and García-Sáez 2014;Schlame et al 2000). While the compositions listed in Table 4 are obtained from healthy cells or tissues, changes in the membrane lipid compositions during apoptosis have also been well documented (Crimi and Degli Esposti 2011;Jourdain and Martinou 2009). In particular, the changes following stimulation of the extrinsic or intrinsic pathways have been compiled in various cell systems and reviewed in detail (Crimi and Degli Esposti 2011).…”

Section: The Role Of Mitochondrial Membrane Lipids In Mompmentioning

confidence: 99%

Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization

et al. 2017

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Apoptosis is important in regulating cell death turnover and is mediated by the intrinsic and death receptor-based extrinsic pathways which converge at the mitochondrial outer membrane (MOM) leading to mitochondrial outer membrane permeabilization (MOMP). MOMP results in the release of apoptotic proteins that further activate the downstream pathway of apoptosis. Thus, tight regulation of MOMP is crucial in controlling apoptosis, and a lack of control may lead to tissue and organ malformation and the development of cancers. Despite a growing number of studies focusing on the structure and activity of the proteins involved in mediating MOMP, such as the Bcl-2 family proteins, the mechanism of MOMP is not well understood. In particular, the crucial role of the various structural properties and changes in lipid components of the MOM in mediating the recruitment and activation of different Bcl-2 proteins remains poorly understood. Furthermore, the factors that control the changes in mitochondrial membrane integrity from the initiation to the final disruption of MOM have yet to be clearly defined. In this review, we provide an overview of studies that focus on the mitochondrial membrane with a biophysical analysis of the interactions of the Bcl-2 proteins with the mitochondrial membrane.

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Mitochondrial outer-membrane permeabilization and remodelling in apoptosis

Cited by 108 publications

References 98 publications

Neonatal monocytes express antiapoptotic pattern of Bcl-2 proteins and show diminished apoptosis upon infection with Escherichia coli

Neonatal monocytes express antiapoptotic pattern of Bcl-2 proteins and show diminished apoptosis upon infection with Escherichia coli

Millimeter wave radiation induces apoptosis via affecting the ratio of Bax/Bcl-2 in SW1353 human chondrosarcoma cells

Mitochondrial outer membrane permeabilization: a focus on the role of mitochondrial membrane structural organization

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