The establishment of a reliable cytotoxic system with SK-N-SH neuroblastoma cell culture

Ba, Fang; Pang, Peter K.T.; Benishin, Christina G.

doi:10.1016/s0165-0270(02)00324-2

Cited by 44 publications

(33 citation statements)

References 29 publications

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“…The tyrosine kinase inhibitor genistein and the p60 (Src) tyrosinespecific kinase inhibitor prevent the H 2 O 2 -and the parkinsonian toxin 1-methyl-4-phenylpyridinium-induced apoptosis in mesencephalic dopaminergic neuronal cell line [16]. In contrast to these reports, the protein tyrosine kinase inhibitor tyrphostin AG18 does not inhibit the b-amyloid protein-, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-, or serum deprivation-induced cell death in SK-N-SH neuroblastoma cell line [17]. Furthermore, tyrphostin AG47 markedly increases cell death during oxygen-glucose deprivation [18].…”

Section: Introductioncontrasting

confidence: 62%

Tyrosine Kinase Inhibitor AG126 Reduces 7-Ketocholesterol-Induced Cell Death by Suppressing Mitochondria-Mediated Apoptotic Process

Kim

Lee

2009

Neurochem Res

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The preventive effect of tyrosine kinase inhibitor AG126 against the 7-ketocholesterol toxicity was investigated in relation to the mitochondria-mediated cell death process. 7-Ketocholesterol induced the nuclear damage, the mitochondrial membrane permeability changes, the formation of reactive oxygen species and the depletion of GSH, which leads to cell death in differentiated PC12 cells. Tyrphostin AG126 significantly attenuated the 7-ketocholesterol-induced decrease in cytosolic Bid and Bcl-2 levels, increase in cytosolic pro-apoptotic Bax levels, mitochondrial membrane potential loss, cytochrome c release and subsequent caspase-3 activation. The inhibitory effect of tyrphostin AG126 may be supported by the inhibitory effect on another oxysterol 25-hydroxycholesterol-induced cell death. The results show that tyrphostin AG126 may prevent the 7-ketocholesterol toxicity by suppressing the mitochondrial membrane permeability change that leads to the cytochrome c release and caspase-3 activation. The preventive effect seems to be associated with the inhibitory effect on the formation of reactive oxygen species and the depletion of GSH.

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Section: Introductioncontrasting

confidence: 62%

Tyrosine Kinase Inhibitor AG126 Reduces 7-Ketocholesterol-Induced Cell Death by Suppressing Mitochondria-Mediated Apoptotic Process

Kim

Lee

2009

Neurochem Res

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“…SK-N-SH cells exhibit a neuronal phenotype and have been used extensively to assess potential neuroprotective mechanisms against numerous insults including serum deprivation [1]. To this end, cells were incubated for 48 hr with and without serum and treated with VEGF and a selective inhibitor of p38 MAPK, SB202190 either alone or in combination (Fig.…”

Section: Resultsmentioning

confidence: 99%

p38 MAPK as a negative regulator of VEGF/VEGFR2 signaling pathway in serum deprived human SK-N-SH neuroblastoma cells

Gomes

Rockwell

2008

Neuroscience Letters

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Evidence suggests that vascular endothelial growth factor (VEGF) mediates neuroprotection to prevent an apoptotic cell death. The p38 mitogen activated protein kinase (MAPK) pathway is implicated as an important mediator of neuronal apoptosis but its role in VEGF-mediated neuroprotection is unclear. Herein, we show that treatments with the p38 MAPK inhibitor, SB202190, enhanced VEGF-mediated survival in serum deprived SK-N-SH neuroblastoma cells by decreasing caspase-3/7 activation while increasing the phosphorylation of the extracellular signalregulated kinase (ERK1/2) and Akt signaled through the VEGF receptor, VEGFR2. A blockade of VEGFR2 signaling with a selective inhibitor, SU1498 or gene silencing with VEGFR2 siRNA in SB202190 treated cells abrogated this prosurvival response and induced high activation levels of caspase-3/7. These findings suggested that the protection elicited by p38 MAPK inhibition in serum starved cells was dependent on a functional VEGF/VEGFR2 pathway. However, p38 MAPK inhibition attenuated caspase-3 cleavage in SU1498/SB202190 treated cells, indicating that p38 MAPK and caspase-3 only contributed in part to the total levels of caspase-3/7 induced by VEGFR2 inhibition. Pretreatments with the pan caspase inhibitor, z-VAD-fmk, prevented the apoptosis induced by VEGFR2 inhibition and promoted survival in serum starved cells irrespective of p38 MAPK inhibition. Collectively, our findings suggest that p38 MAPK exerts a negative effect on VEGF-mediated signaling through VEGFR2 in serum starved neuroblastoma cells. Furthermore, VEGF signals protection against a caspase-mediated cell death that is regulated by p38 MAPKdependent and -independent mechanisms.

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“…SK-N-SH cells exhibit a neuronal phenotype with expression of multiple neurochemical markers [8]. SK-N-SH cells respond to numerous insults including β-amyloid, mitochondrial permeability transition, and serum deprivation, indicating that this cell line could be very useful in the assessment of neurotoxicity and neuroprotection [4]. SK-N-SH cells have been used by this and other laboratories [5,20,21,46,[48][49][50][51]56] as an in vitro model for studying potential neuroprotection mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Pyruvate protects mitochondria from oxidative stress in human neuroblastoma SK-N-SH cells

et al. 2007

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Oxidative stress is implicated in neurodegenerative diseases including stroke, Alzheimer's disease and Parkinson's disease, and has been extensively studied as a potential target for therapeutic intervention. Pyruvate, a natural metabolic intermediate and energy substrate, exerts antioxidant effects in brain and other tissues susceptible to oxidative stress. We tested the protective effects of pyruvate on hydrogen peroxide (H 2 O 2 ) toxicity in human neuroblastoma SK-N-SH cells and the mechanisms underlying its protection. Hydrogen peroxide insult resulted in 85% cell death, but cotreatment with pyruvate dose-dependently attenuated cell death. At concentrations of ≥ 1 mM, pyruvate totally blocked the cytotoxic effects of H 2 O 2 . Pyruvate exerted its protective effects even when its administration was delayed up to 2 hr after H 2 O 2 insult. As a scavenger of reactive oxygen species (ROS), pyruvate dose-dependently attenuated H 2 O 2 -induced ROS formation, assessed from 2,7-dichlorofluorescein diacetate fluorescence. Furthermore, pyruvate suppressed superoxide production by submitochondrial particles, and attenuated oxidative stress-induced collapse of the mitochondrial membrane potential. Collectively, these results suggest pyruvate protects neuronal cells through its antioxidant actions on mitochondria.

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The establishment of a reliable cytotoxic system with SK-N-SH neuroblastoma cell culture

Cited by 44 publications

References 29 publications

Tyrosine Kinase Inhibitor AG126 Reduces 7-Ketocholesterol-Induced Cell Death by Suppressing Mitochondria-Mediated Apoptotic Process

Tyrosine Kinase Inhibitor AG126 Reduces 7-Ketocholesterol-Induced Cell Death by Suppressing Mitochondria-Mediated Apoptotic Process

p38 MAPK as a negative regulator of VEGF/VEGFR2 signaling pathway in serum deprived human SK-N-SH neuroblastoma cells

Pyruvate protects mitochondria from oxidative stress in human neuroblastoma SK-N-SH cells

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