Mitochondrial Dysfunction and Apoptosis Related Gene Expression in A beta(25-35)-Treated Human Neuroblastoma Cell Line, SK-N-SH
Journal of the Korean Geriatrics Society
;
: 142-151, 2009.
Article
in Korean
| WPRIM
| ID: wpr-162533
ABSTRACT
BACKGROUND:
Mitochondrial dysfunction plays an important role in Abeta-induced neuronal toxicity in Alzheimer's disease (AD). We measured the membrane potentials of mitochondria (delta psim) and assessed the genetic expressions of A beta(25-35)-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 micrometer A beta(25-35) for 0-24 hours, and kinetic study was done. delta psim was measured by flow cytometry. Messenger RNA expressions of cytochrome c oxidase (COX), cytochrome c, succinate dehydrogenase (SDH), amyloid-beta 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:
delta psim was reduced at 24 hours. mRNA expression for COX gradually decreased by about 29% (p<0.05) while-expressions 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 A beta(25-35) 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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Succinate Dehydrogenase
/
Alcohol Dehydrogenase
/
RNA, Messenger
/
Gene Expression
/
Cell Line
/
Amyloid beta-Peptides
/
Citric Acid Cycle
/
Cell Death
/
Apoptosis
/
Electron Transport Complex IV
Limits:
Humans
Language:
Korean
Journal:
Journal of the Korean Geriatrics Society
Year:
2009
Type:
Article
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