Modulated induction of tau proteins in cultured human neuroblastoma cells

Ko, Li Wen; Liu, Wan Kyng; Georgieff, Irene S.; Yen, Shu Hui

doi:10.1016/0006-8993(95)01268-0

Cited by 7 publications

(5 citation statements)

References 59 publications

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“…Protein constituents of distinct culture specimens were resolved using the same volume containing an equivalent number of cells by 0.1% sodium dodecyl sulfate‐polyacrylamide gel electrophoresis using 15% gel (Bio‐Rad Laboratories, Hercules, CA, U.S.A.). This was followed by transblotting onto nitrocellulose membranes (Ko et al, 1996). An α‐SN‐enriched human brain preparation was prepared according to Jakes et al (1994) and included as a reference.…”

Section: Methodsmentioning

confidence: 99%

“…Lee (University of Pennsylvania, Philadelphia, PA, U.S.A.) and T. Iwatsubo (University of Tokyo, Tokyo, Japan)] (Baba et al, 1998), and a mouse monoclonal antibody to synuclein‐1 (1:1,000, ascites fluid; Transduction Laboratories, Lexington, KY, U.S.A.). α‐SN immunoreactivity was detected by enhanced chemiluminescence, and its identity was verified by dissecting the transblotted α‐SN longitudinally into strips that were probed with separate α‐SN antibodies independently as described before (Ko et al, 1996, 1997).…”

Section: Methodsmentioning

confidence: 99%

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Sensitization of Neuronal Cells to Oxidative Stress with Mutated Human α‐Synuclein

Mehta

Farrer

et al. 2000

Journal of Neurochemistry

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Linkage of ␣-synuclein (␣-SN) mutations to familial Parkinson's disease (PD) and presence of ␣-SN as a major constituent of Lewy body in both sporadic and familial PD implicate ␣-SN abnormality in PD pathogenesis. Here we demonstrate that overexpression of wildtype or mutant ␣-SN does not cause any deleterious effect on the growth or continued propagation of transfected human cells, but overproduction of mutant ␣-SN heightens their sensitivity to menadione-induced oxidative injury. Such enhanced vulnerability is more pronounced in neuronal transfectants than in their nonneuronal counterparts and is associated with increased production of reactive oxygen species. The data suggest that mutated ␣-SN, especially with an alanine-to-proline substitution at residue 30, sensitizes neuronal cells to oxidative damage. Key Words: ␣-Synuclein-Oxidative stress-Menadione-Parkinson's disease.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Sensitization of Neuronal Cells to Oxidative Stress with Mutated Human α‐Synuclein

Mehta

Farrer

et al. 2000

Journal of Neurochemistry

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“…In this study, a bioinformatics approach was first applied on extracted compounds reported by Dou et al [18] and thereafter picein was opted for use in in vitro studies due to its strong role in the treatment of AD. In vitro studies were performed on SH-SY5Y neuroblastoma cells because of their close resemblance to neurons and they are accepted as a unique model for neurodegenerative diseases [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Plant-Derived Natural Biomolecule Picein Attenuates Menadione Induced Oxidative Stress on Neuroblastoma Cell Mitochondria

et al. 2020

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Several bioactive compounds are in use for the treatment of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease. Historically, willow (salix sp.) bark has been an important source of salisylic acid and other natural compounds with anti-inflammatory, antipyretic and analgesic properties. Among these, picein isolated from hot water extract of willow bark, has been found to act as a natural secondary metabolite antioxidant. The aim of this study was to investigate the unrevealed pharmacological action of picein. In silico studies were utilized to direct the investigation towards the neuroprotection abilities of picein. Our in vitro studies demonstrate the neuroprotective properties of picein by blocking the oxidative stress effects, induced by free radical generator 2-methyl-1,4-naphthoquinone (menadione, MQ), in neuroblastoma SH-SY5Y cells. Several oxidative stress-related parameters were evaluated to measure the protection for mitochondrial integrity, such as mitochondrial superoxide production, mitochondrial activity (MTT), reactive oxygen species (ROS) and live-cell imaging. A significant increase in the ROS level and mitochondrial superoxide production were measured after MQ treatment, however, a subsequent treatment with picein was able to mitigate this effect by decreasing their levels. Additionally, the mitochondrial activity was significantly decreased by MQ exposure, but a follow-up treatment with picein recovered the normal metabolic activity. In conclusion, the presented results demonstrate that picein can significantly reduce the level of MQ-induced oxidative stress on mitochondria, and thereby plays a role as a potent neuroprotectant.

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“…SH-SY5Y cells are similar to neurones and are a widely used neurodegenerative diseases model. Therefore, SH-SY5Y cells were used in this research [ 20 ]. To reveal the molecular mechanism, SH-SY5Y cells were treated with 6-OHDA, an effective dopamine-induced neuronal degeneration nerve agent that can induce mitochondrial damage, chronic oxidative stress, and cell death.…”

Section: Introductionmentioning

confidence: 99%

Vitamin K2 Modulates Mitochondrial Dysfunction Induced by 6-Hydroxydopamine in SH-SY5Y Cells via Mitochondrial Quality-Control Loop

et al. 2022

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Vitamin K2, a natural fat-soluble vitamin, is a potent neuroprotective molecule, owing to its antioxidant effect, but its mechanism has not been fully elucidated. Therefore, we stimulated SH-SY5Y cells with 6-hydroxydopamine (6-OHDA) in a proper dose-dependent manner, followed by a treatment of vitamin K2. In the presence of 6-OHDA, cell viability was reduced, the mitochondrial membrane potential was decreased, and the accumulation of reactive oxygen species (ROS) was increased. Moreover, the treatment of 6-OHDA promoted mitochondria-mediated apoptosis and abnormal mitochondrial fission and fusion. However, vitamin K2 significantly suppressed 6-OHDA-induced changes. Vitamin K2 played a significant part in apoptosis by upregulating and downregulating Bcl-2 and Bax protein expressions, respectively, which inhibited mitochondrial depolarization, and ROS accumulation to maintain mitochondrial structure and functional stabilities. Additionally, vitamin K2 significantly inhibited the 6-OHDA-induced downregulation of the MFN1/2 level and upregulation of the DRP1 level, respectively, and this enabled cells to maintain the dynamic balance of mitochondrial fusion and fission. Furthermore, vitamin K2 treatments downregulated the expression level of p62 and upregulated the expression level of LC3A in 6-OHDA-treated cells via the PINK1/Parkin signaling pathway, thereby promoting mitophagy. Moreover, it induced mitochondrial biogenesis in 6-OHDA damaged cells by promoting the expression of PGC-1α, NRF1, and TFAM. These indicated that vitamin K2 can release mitochondrial damage, and that this effect is related to the participation of vitamin K2 in the regulation of the mitochondrial quality-control loop, through the maintenance of the mitochondrial quality-control system, and repair mitochondrial dysfunction, thereby alleviating neuronal cell death mediated by mitochondrial damage.

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Modulated induction of tau proteins in cultured human neuroblastoma cells

Cited by 7 publications

References 59 publications

Sensitization of Neuronal Cells to Oxidative Stress with Mutated Human α‐Synuclein

Sensitization of Neuronal Cells to Oxidative Stress with Mutated Human α‐Synuclein

Plant-Derived Natural Biomolecule Picein Attenuates Menadione Induced Oxidative Stress on Neuroblastoma Cell Mitochondria

Vitamin K2 Modulates Mitochondrial Dysfunction Induced by 6-Hydroxydopamine in SH-SY5Y Cells via Mitochondrial Quality-Control Loop

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