Uptake of a neurotoxin-candidate, (R)-1,2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline into human dopaminergic neuroblastoma SH-SY5Y cells by dopamine transport system

Takahashi, Tsutomu; Deng, Yulin; Maruyama, Wakako; Dostert, P.; Kawai, Maki; Naoi, Makoto

doi:10.1007/bf01277014

Cited by 93 publications

(46 citation statements)

References 25 publications

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“…In the present study, we have tested the ability of VPA in neuroprotection against rotenone-induced apoptosis in SH-SY5Y, a human DAergic cell line often used for study of neurodegeneration mechanisms relevant to PD [15][16][17]. By using this rotenone-induced apoptosis cell model, we have evaluated the role of Hsp70 and several critical signaling pathways involved in VPA-mediated neuroprotection.…”

Section: Introductionmentioning

confidence: 99%

Valproic acid‐mediated Hsp70 induction and anti‐apoptotic neuroprotection in SH‐SY5Y cells

Pan

Xie

et al. 2005

FEBS Letters

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Valproic acid (VPA), an anticonvulsant and moodstabilizing drug, has been reported to exert neuroprotection against a variety of insults. We now show that VPA attenuates rotenone (a potent complex I inhibitor)-induced apoptosis through the induction of heat shock protein 70, which may interact with apoptotic-protease-activating factor 1. Activation of p-Akt, p-Bcl-2, as well as p-Erk1/2 by VPA may be co-contributors to the protection.

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Section: Introductionmentioning

confidence: 99%

Valproic acid‐mediated Hsp70 induction and anti‐apoptotic neuroprotection in SH‐SY5Y cells

Pan

Xie

et al. 2005

FEBS Letters

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“…S1P significantly enhanced cell viability mainly by activation of S1P1 receptor mediated signalling [41]. In our previous and in this study we used human dopaminergic SH-SY5Y cells, because they express tyrosine hydroxylase (HT), dopamine β-hydroxylase (DBH) [38] and the dopamine transporter (DAT) [24,51,59] and have been widely used to gain a better understanding of the molecular processes and pathomechanism of PD. In the present study we investigated gene expression for Sphk1/2 and for enzymes involved in S1P degradation (SPL and SPP).…”

Section: Introductionmentioning

confidence: 99%

Original article The key role of sphingosine kinases in the molecular mechanism of neuronal cell survival and death in an experimental model of Parkinson’s disease

Pyszko¹,

Strosznajder²

2014

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“…Izabrana ćelijska linija pokazuje neke karakteristike dopaminergičkih neurona -mogućnost sinteze dopamina i noradrenalina usled ekspresije dopamin-i tirozin-β-hidroksilaze (16) i ekspresiju transportera dopamina (DAT) na membrani (17). Diferencijacija ćelija do neurona izvršena je "all-trans" retinoičnom kiselinom (engl.…”

Section: Materijal I Metode Kultura ćElija I Reagensiunclassified

The role of autophagy in neurotoxicity caused by extracellular ASYN

Djuranovic¹,

Jeremic²,

Zogović³

et al. 2016

Med podmladak

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Key words:α-synuclein, autophagy, ATG7, SH-SY5Y, neurotoxicityIntroduction: The accumulation of alpha-synuclein (ASYN) in susceptible neurons is considered to be a major contributing factor in pathogenesis of Parkinson's disease. Although ASYN was considered as an intracellular protein, recent data suggest that it can be detected extracellularly. Autophagy plays an important role in ASYN degradation; therefore, impairment of autophagy could be an important contributor to ASYN accumulation. ATG (autophagy-related genes) proteins function at several physiologically continuous steps in autophagy, and ATG7 is considered as essential in autophagosome formation and maturation. Aim: The aim of this study was to investigate the role of autophagy in neurotoxicity, caused by extracellular ASYN. Material and methods: All experiments were conducted in all-trans retinoic acid-differentiated human neuroblastoma SH-SY5Y cells, that were exposed to extracellular ASYN. The presence of extracellular ASYN and the expression of autophagy markers, beclin-1 and LC3-II, were monitored using immunoblotting. Transfection, with small interfering RNA (siRNA), was used to knock down ATG7 gene. Cell viability was assessed using crystal violet dye exclusion assay. Results: Extracellular ASYN caused significant loss of viability in differentiated SH-SY5Y cells, accompanied by the increase in expression of beclin-1 and in conversion of LC3-I to autophagosome-associated LC3-II. The RNA interference-mediated knock-down of ATG7 increased the sensitivity of SH-SY5Y cells to the extracellular ASYN-induced toxicity. Conclusion: Extracellular ASYN caused loss of viability in differentiated SH-SY5Y cells accompanied by autophagy induction. Having in mind that inhibition of autophagy, through ATG7 knock-down increased cell death, we can conclude that autophagy could have a protective role in the harmful effect of extracellular ASYN.

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Uptake of a neurotoxin-candidate, (R)-1,2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline into human dopaminergic neuroblastoma SH-SY5Y cells by dopamine transport system

Cited by 93 publications

References 25 publications

Valproic acid‐mediated Hsp70 induction and anti‐apoptotic neuroprotection in SH‐SY5Y cells

Valproic acid‐mediated Hsp70 induction and anti‐apoptotic neuroprotection in SH‐SY5Y cells

Original article The key role of sphingosine kinases in the molecular mechanism of neuronal cell survival and death in an experimental model of Parkinson’s disease

The role of autophagy in neurotoxicity caused by extracellular ASYN

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