Modifications of Ca2+Mobilization and Noradrenaline Release byS-Nitroso-cysteine in PC12 Cells1

Naganuma, Takao; Murayama, Toshihiko; Nomura, Yasuyuki

doi:10.1006/abbi.1999.1075

Cited by 25 publications

(11 citation statements)

References 43 publications

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“…Isolated PC12 cells were loaded with 2 mM fura-2/AM to 1 lM/10 7 cells in Tyrode I solution (137 mM NaCl, 5 mM KCl, 5 mM glucose, 1 mM MgCl 2 , 1 mM CaCl 2 , 0.2% BSA and 20 mM HEPES, pH 7.4) for 30 min at 37°C [24]. PC12 cells were washed twice with Tyrode II solution (in mM: NaCl 137, KCl 5, glucose 5, MgCl 2 1 and HEPES 20, pH 7.4) by centrifugation at 412 · g for 10 min and suspended in the same solution.…”

Section: Measurement Of Intracellular Calcium Levelsmentioning

confidence: 99%

Differential Involvement of Intracellular Ca2+ in 1-Methyl-4-phenylpyridinium- or 6-Hydroxydopamine-Induced Cell Viability Loss in PC12 Cells

Lee

Han

et al. 2006

Neurochem Res

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1-Methyl-4-phenylpyridinium (MPP(+)) or 6-hydroxydopamine (6-OHDA) caused a nuclear damage, the mitochondrial membrane permeability changes, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species and the depletion of GSH in PC12 cells. Nicardipine (a calcium channel blocker), EGTA (an extracellular calcium chelator), BAPTA-AM (a cell permeable calcium chelator) and calmodulin antagonists (W-7 and calmidazolium) attenuated the MPP(+)-induced mitochondrial damage and cell death. In contrast, the compounds did not reduce the toxicity of 6-OHDA. Treatment with MPP(+ )or 6-OHDA evoked the elevation of intracellular Ca(2+) levels. Unlike cell injury, addition of nicardipine, BAPTA-AM and calmodulin antagonists prevented the elevation of intracellular Ca(2+) levels due to both toxins. The results show that the MPP(+)-induced formation of the mitochondrial permeability transition seems to be mediated by elevation of intracellular Ca(2+) levels and calmodulin action. In contrast, the 6-OHDA-induced cell death seems to be mediated by Ca(2+)-independent manner.

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Section: Measurement Of Intracellular Calcium Levelsmentioning

confidence: 99%

Differential Involvement of Intracellular Ca2+ in 1-Methyl-4-phenylpyridinium- or 6-Hydroxydopamine-Induced Cell Viability Loss in PC12 Cells

Lee

Han

et al. 2006

Neurochem Res

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“…Dendritic cells were loaded with 2 mM fura 2-AM to 1 μM/10 7 cells in Tyrode I solution (137 mM NaCl, 5 mM KCl, 5 mM glucose, 1 mM MgCl 2 , 1 mM CaCl 2 , 0.2% fetal bovine serum and 20 mM HEPES, pH 7.4) for 30 min at 37°C [22]. Cells were washed twice with Tyrode II solution (in mM: NaCl 137, KCl 5, glucose 5, MgCl 2 1 and HEPES 20, pH 7.4) by centrifugation at 412 × g for 10 min and suspended in the same solution.…”

Section: Measurement Of Intracellular Ca 2+ Levels With the Dye Fura-mentioning

confidence: 99%

Inhibition of activated responses in dendritic cells exposed to lipopolysaccharide and lipoteichoic acid by diarylheptanoid oregonin

Choi

Lee

et al. 2008

International Immunopharmacology

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“…Measurement of intracellular Ca 2+ levels with the dye fura-2/AM Isolated PC12 cells were loaded with 2 mM fura-2/AM to 1 lM/10 7 cells in Tyrode I solution (137 mM NaCl, 5 mM KCl, 5 mM glucose, 1 mM MgCl 2 , 1 mM CaCl 2 , 0.2% BSA, and 20 mM HEPES, pH 7.4) for 30 min at 37°C [26]. PC12 cells were washed twice with Tyrode II solution (in mM: NaCl 137, KCl 5, glucose 5, MgCl 2 1, and HEPES 20, pH 7.4) by centrifugation at 412·g for 10 min and suspended in the same solution.…”

Section: Measurement Of Apoptosis In Cells By Measuring Dna Fragmentamentioning

confidence: 99%

Differential Modulation of 7-Ketocholesterol Toxicity Against PC12 Cells by Calmodulin Antagonists and Ca2+ Channel Blockers

et al. 2006

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The present study assessed the influence of intracellular Ca2+ and calmodulin against the neurotoxicity of oxysterol 7-ketocholesterol in relation to the mitochondria-mediated cell death process and oxidative stress in PC12 cells. Calmodulin antagonists calmidazolium and W-7 prevented the 7-ketocholesterol-induced mitochondrial damage, leading to caspase-3 activation and cell death, whereas Ca2+ channel blocker nicardipine, mitochondrial Ca2+ uptake inhibitor ruthenium red, and cell permeable Ca2+ chelator BAPTA-AM did not reduce it. Exposure of PC12 cells to 7-ketocholesterol caused elevation of intracellular Ca2+ levels. Unlike cell injury, calmodulin antagonists, nicardipine, and BAPTA-AM prevented the 7-ketocholesterol-induced elevations of intracellular Ca2+ levels. The results show that the cytotoxicity of 7-ketocholesterol seems to be modulated by calmodulin rather than changes in intracellular Ca2+ levels. Calmodulin antagonists may prevent the cytotoxicity of 7-ketocholesterol by suppressing the mitochondrial permeability transition formation, which is associated with the increased formation of reactive oxygen species and the depletion of GSH.

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Modifications of Ca2+Mobilization and Noradrenaline Release byS-Nitroso-cysteine in PC12 Cells1

Cited by 25 publications

References 43 publications

Differential Involvement of Intracellular Ca2+ in 1-Methyl-4-phenylpyridinium- or 6-Hydroxydopamine-Induced Cell Viability Loss in PC12 Cells

Differential Involvement of Intracellular Ca2+ in 1-Methyl-4-phenylpyridinium- or 6-Hydroxydopamine-Induced Cell Viability Loss in PC12 Cells

Inhibition of activated responses in dendritic cells exposed to lipopolysaccharide and lipoteichoic acid by diarylheptanoid oregonin

Differential Modulation of 7-Ketocholesterol Toxicity Against PC12 Cells by Calmodulin Antagonists and Ca2+ Channel Blockers

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