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KMID : 0828520090130030142
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Journal of the Korean Geriatrics Society
2009 Volume.13 No. 3 p.142 ~ p.151
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Mitochondrial Dysfunction and Apoptosis Related Gene Expression in Aβ25-35-Treated Human Neuroblastoma Cell Line, SK-N-SH
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Choi Young-Sook
Kim Sang-Ho
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Abstract
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Background: Mitochondrial dysfunction plays an important role in Aβ-induced neuronal toxicity in Alzheimer`s disease (AD). We measured the membrane potentials of mitochondria (△Ψm) and assessed the genetic expressions of Aβ25-35- induced neurotoxicity in the human neuroblastoma cell line, SK-N-SH cell.
Methods: SK-N-SH cells were incubated with a single dose of 25 μM Aβ25-35 for 0-24 hours, and kinetic study was done. △Ψm was measured by flow cytometry. Messenger RNA expressions of cytochrome c oxidase (COX), cytochrome c, succinate dehydrogenase (SDH), amyloid-β alcohol dehydrogenase (ABAD), caspase 9, and Bcl-2 were measured by quantitative real-time reverse transcriptase polymerase chain reaction (real-time RT-PCR). Cell death rate was measured by MTT reduction assay.
Results: △Ψm was reduced at 24 hours. mRNA expression for COX gradually decreased by about 29%(p<0.05) whileexpressions for cytochrome c, SDH, ABAD, and caspase 9 increased (p<0.05) progressively during the 24-hour time period. Bcl-2 expression decreased (p<0.05) gradually; and apoptotic cell death rate was about 24%(p<0.01) by 24 hours.
Conclusion: Extracellular administration of Aβ25-35 contributes directly to mitochondrial dysfunction in SK-N-SH cells with the enzymatic impairment of the tricarboxylic acid cycle and electron transport chain, and eventually leading to apoptotic cell death.
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KEYWORD
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Amyloid beta-protein, Apoptosis, Caspase 9, Cytochrome c, Electron transport complex IV, Membrane potentials, Mitochondria
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