Role of Bcl-2 family of proteins in mediating apoptotic death of PC12 cells exposed to oxygen and glucose deprivation

Koubi, David; Jiang, Hao; Zhang, Lijie; Tang, Wenxue; Kuo, Jarret; Rodríguez, A Herrera; Hunter, Tangella Jackson; Seidman, Michael D.; Corcoran, George B.; Levine, Robert A.

doi:10.1016/j.neuint.2004.06.006

Cited by 27 publications

(13 citation statements)

References 35 publications

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“…PC12 cells are subjected to an initial short phase of OGD followed by a prolonged phase of oxygen and glucose restoration (adding back oxygen and glucose). The initial phase of OGD mimics the lack of oxygen and glucose supply such as a thrombus formation during stroke, while the prolonged phase of oxygen and glucose restoration reflects the reperfusion of oxygen and glucose supply to the injured brain (Koubi et al 2005;Tabakman et al 2005). Using the in vitro OGD model of PC12 cultures, we found that the viability of PC12 cells was markedly decreased to 56.2 ± 5.7% after OGD insult, suggesting a high sensitivity to this type of insult.…”

Section: Discussionmentioning

confidence: 88%

TAT-Mediated Protein Transduction of Nogo Extracellular Peptide 1-40 and its Biological Activity

et al. 2008

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These results demonstrate that the TAT-NEP1-40 can be successfully generated and efficiently transduced into PC12 cells and rat brains. The TAT-NEP1-40 can protect PC12 cells against OGD and promote neurite outgrowth. This finding suggests that the transducible TAT-NEP1-40 fusion protein offers a possibility of the development of novel therapy for cerebral injuries via delivery of the biologically active TAT-NEP1-40 fusion protein into injured sites.

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Section: Discussionmentioning

confidence: 88%

TAT-Mediated Protein Transduction of Nogo Extracellular Peptide 1-40 and its Biological Activity

et al. 2008

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“…In the process of ischemia, the Bcl-2 family of proteins, which consists of anti-apoptotic proteins of Bcl-2 and proapoptotic proteins of Bax, could mediate apoptosis by opening of mitochondrial permeability transition pore marked with the collapse of MMP, and down-regulation of the ratio of Bcl-2 to Bax has been reported to be correlated with the collapse of MMP [28,29] . The opening of the mitochondrial permeability transition pore causes a release of pro-apoptotic proteins such as cytochrome c from mitochondria into cytoplasm [30] , and then, cytochrome c will bind to apoptotic protease-activating factor-1, and support the catalytic activation of caspase-9, which further cleaves and activates the effector caspase-3 resulting in the subsequent apoptosis event.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of ginsenoside Rb3 on oxygen and glucose deprivation-induced ischemic injury in PC12 cells

et al. 2010

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Aim: To investigate the protective effects of ginsenoside Rb 3 , a triterpenoid saponin isolated from the leaves of Panax notoginseng, on ischemic and reperfusion injury model of PC12 cells and elucidate the related mechanisms. Methods: PC12 cells exposed to oxygen and glucose deprivation (OGD) and restoration (OGD-Rep) were used as an in vitro model of ischemia and reperfusion. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) leakage were used to evaluate the protective effects of ginsenoside Rb 3 . Cellular apoptosis and mitochondrial membrane potential (MMP) were analyzed using flow cytometry. Intracellular calcium ion concentration ([Ca 2+ ] i ) was detected using fluorophotometer system. Caspase-3, -8, and -9 activities were measured using assay kits with an ELISA reader. Western blotting assay was used to evaluate the release of cytochrome c and expression of caspase-3, Bcl-2 and Bax proteins. Results: It was shown that ginsenoside Rb 3 (0.1-10 μmol/L) significantly increased cell viability and inhibited LDH release in a dosedependent manner on the ischemic model. In addition, ginsenoside Rb 3 also significantly inhibited ischemic injury-induced apoptosis, [Ca 2+ ] i elevation, and decrease of MMP. Meanwhile, pretreatment with ginsenoside Rb 3 significantly induced an increase of Bcl-2 protein expression and a decrease of cytosolic cytochrome c, cleaved-caspase 3 and Bax protein expression, the caspase-3, -8, and -9 activity were also inhibited. Conclusion:The results indicated that ginsenoside Rb 3 could markedly protected OGD-Rep induced ischemic injury and the mechanisms maybe related to its suppression of the intracellular Ca 2+ elevation and inhibition of apoptosis and caspase activity. Ginsenoside Rb 3 could be a promising candidate in the development of a novel class of anti-ischemic agent.

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“…The collected cells were rinsed with PBS, and incubated with 1 mol/l rhodamine 123 in PBS at 37 ° C for 60 min in the dark. The cells stained with rhodamine 123 were analyzed as described previously [33] using a flow cytometer EPICS XL-MCL System II (Beckman Coulter, Inc., Fullerton, Calif., USA).…”

Section: Measurement Of Mitochondrial Membrane Potentialmentioning

confidence: 99%

Desipramine Induces Apoptotic Cell Death through Nonmitochondrial and Mitochondrial Pathways in Different Types of Human Colon Carcinoma Cells

Arimochi

Morita

2007

Pharmacology

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Cytotoxic effects of desipramine on human colon carcinoma HT29 and HCT116 cells were examined. Desipramine reduced the viability of HT29 cells in a concentration-dependent manner, but failed to cause any significant change in the viability of HCT116 cells by the concentration up to 50 µmol/l, at which an approximately 60% reduction of the viability of HT29 cells was observed. Despite their different sensitivities, desipramine caused the nonoxidative apoptotic damage to both of them. In contrast to HT29 cells, desipramine might cause the apoptotic death of HCT116 cells through the disturbance of mitochondrial function. These results suggest that desipramine may cause the nonoxidative apoptotic damage to different types of human colon carcinoma cells through either a nonmitochondrial or a mitochondrial pathway, which may confer the different sensitivities to this drug on these tumor cells.

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Role of Bcl-2 family of proteins in mediating apoptotic death of PC12 cells exposed to oxygen and glucose deprivation

Cited by 27 publications

References 35 publications

TAT-Mediated Protein Transduction of Nogo Extracellular Peptide 1-40 and its Biological Activity

TAT-Mediated Protein Transduction of Nogo Extracellular Peptide 1-40 and its Biological Activity

Protective effects of ginsenoside Rb3 on oxygen and glucose deprivation-induced ischemic injury in PC12 cells

Desipramine Induces Apoptotic Cell Death through Nonmitochondrial and Mitochondrial Pathways in Different Types of Human Colon Carcinoma Cells

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