MPTP-Induced Modulation of Neurotransmitters in SH-SY5Y Human Neuroblastoma Cells

1998 ◽  
Vol 17 (6) ◽  
pp. 677-701 ◽  
Author(s):  
Xiaoou Song ◽  
Marion Ehrich
Keyword(s):  
Cell Line ◽  
Neuroblastoma Cells ◽  
Neuronal Cell ◽  
Cholinergic Antagonists ◽  
Mao Inhibitor ◽  
Human Neuroblastoma ◽  
Hydroxyindoleacetic Acid ◽  
Mao Activity

Neurotoxic effects of MPTP(1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine) were evaluated in vitro using a human neuronal cell line, SH-SY5Y, that contained features contributing to expression of MPTP toxicity in vivo, namely, a transport system for dopam ine (DA) and monam ine oxidase (MAO) activity. In this model system, MPTP was found to reduce levels of catecholamines (DA, norepinephrine, epinephrine), serotonin (5-HT), and the 5-HT metabolite 5-hydroxyindoleacetic acid (5-HIAA). MPTP enhanced 3H-DA release, which could contribute to the reduction in DA concentrations seen in these cells. In addition, MPTP inhibited MAO activity (Ki 2.26 X 10-5 M). Pretreatment with the MAO inhibitor pargy-line protected the cells from MPTP-induced alterations of catecholamines and the decrease in 5-HT. In this in vitro model, the cholinergic antagonists atro-pine and A-tubocurarine also protected cells from MPTP-induced alterations of catecholamines. The capability of cholinergic antagonists to prevent the MPTP-induced alterations of catecholamine concentrations suggests a possible cholinergic contribution to MPTP neurotoxicity in this cell line.

Expression of trkA cDNA in neuroblastomas mediates differentiation in vitro and in vivo

1993 ◽  
Vol 13 (12) ◽  
pp. 7447-7456
Author(s):  
H Matsushima ◽  
E Bogenmann
Keyword(s):  
Cell Differentiation ◽  
Cell Line ◽  
Neuronal Cell ◽  
Human Neuroblastoma ◽  
Myc Oncogene ◽  
Ngf Receptor ◽  
Neuronal Cell Differentiation ◽  
Mature Neurons

The human trkA cDNA was transfected into a malignant human neuroblastoma (NB) cell line (HTLA230) to investigate its role in NB growth and differentiation. This cell line lacks expression of both endogenous trkA and gp75NGFR genes. Transfectants expressing the trkA mRNA and surface-bound receptors transcriptionally activate immediate-early genes (c-fos, c-jun, and jun-B) following nerve growth factor (NGF) stimulation. NGF treatment induces growth arrest as well as down-regulation of the amplified N-myc oncogene. Genes selectively expressed in mature neurons (SCG-10, ret proto-oncogene, GAP-43, etc.) are transcriptionally activated, and neurite outgrowth further demonstrates differentiation of transfectants following NGF stimulation. trkA-expressing NB cells remain tumorigenic in nude mice; however, subcutaneous treatment of tumor-bearing mice with NGF induces Schwannian and neuronal cell differentiation similar to the induction seen in human ganglioneuroblastomas. Thus, trkA expression in HTLA230 cells is sufficient to generate a functional NGF receptor complex that leads to growth-arrested and differentiated NB cells in vitro and in vivo in the presence of NGF. Hence, NGF may play a crucial role in NB cell differentiation and regression in vivo.

Toxicity of Ethylene-bis-dithiocarbamates (EBDCs) in a Human Neuroblastoma Cell Line

1991 ◽  
Vol 19 (1) ◽  
pp. 39-40
Author(s):  
Dario Cova ◽  
Pietro Fumagalli ◽  
Angela Santagostino
Keyword(s):  
Cell Line ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Neuronal Cell ◽  
Human Cell Line ◽  
Neuroblastoma Cell Line ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Order Of Magnitude

The aim of our research was the in vitro evaluation of the neurotoxic effects of three EBDCs (Nabam, Zineb and Maneb) and ETU on SK-N-BE human neuroblastoma cells as a model for neurotoxicity in humans. The EC50 value was used as an index of the toxicities of these compounds. Since Zineb and Maneb contain zinc and manganese as cations, respectively, in order to determine the contributions of these metals, the EC50s of zinc chloride and manganese chloride were also evaluated. Nabam, Zineb and Maneb had EC50 values ranging from 1μM to 30μM; the EC50s of manganese and zinc in this human cell line were found to be of the same order of magnitude as those of the EBDC fungicides. These in vitro effects are discussed in relation to the possible use of neuronal cell lines for detecting the neurotoxicities of these compounds.

scholarly journals Expression of trkA cDNA in neuroblastomas mediates differentiation in vitro and in vivo.

1993 ◽  
Vol 13 (12) ◽  
pp. 7447-7456 ◽  
Author(s):  
H Matsushima ◽  
E Bogenmann
Keyword(s):  
Cell Differentiation ◽  
Cell Line ◽  
Neuronal Cell ◽  
Human Neuroblastoma ◽  
Myc Oncogene ◽  
Ngf Receptor ◽  
Neuronal Cell Differentiation ◽  
Mature Neurons

The human trkA cDNA was transfected into a malignant human neuroblastoma (NB) cell line (HTLA230) to investigate its role in NB growth and differentiation. This cell line lacks expression of both endogenous trkA and gp75NGFR genes. Transfectants expressing the trkA mRNA and surface-bound receptors transcriptionally activate immediate-early genes (c-fos, c-jun, and jun-B) following nerve growth factor (NGF) stimulation. NGF treatment induces growth arrest as well as down-regulation of the amplified N-myc oncogene. Genes selectively expressed in mature neurons (SCG-10, ret proto-oncogene, GAP-43, etc.) are transcriptionally activated, and neurite outgrowth further demonstrates differentiation of transfectants following NGF stimulation. trkA-expressing NB cells remain tumorigenic in nude mice; however, subcutaneous treatment of tumor-bearing mice with NGF induces Schwannian and neuronal cell differentiation similar to the induction seen in human ganglioneuroblastomas. Thus, trkA expression in HTLA230 cells is sufficient to generate a functional NGF receptor complex that leads to growth-arrested and differentiated NB cells in vitro and in vivo in the presence of NGF. Hence, NGF may play a crucial role in NB cell differentiation and regression in vivo.

scholarly journals A natural product inhibits the initiation of α-synuclein aggregation and suppresses its toxicity

2017 ◽  
Vol 114 (6) ◽  
pp. E1009-E1017 ◽  
Author(s):  
Michele Perni ◽  
Céline Galvagnion ◽  
Alexander Maltsev ◽  
Georg Meisl ◽  
Martin B. D. Müller ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Natural Product ◽  
Self Assembly ◽  
Lipid Membranes ◽  
Neuroblastoma Cells ◽  
Lipid Vesicles ◽  
Human Neuroblastoma

The self-assembly of α-synuclein is closely associated with Parkinson’s disease and related syndromes. We show that squalamine, a natural product with known anticancer and antiviral activity, dramatically affects α-synuclein aggregation in vitro and in vivo. We elucidate the mechanism of action of squalamine by investigating its interaction with lipid vesicles, which are known to stimulate nucleation, and find that this compound displaces α-synuclein from the surfaces of such vesicles, thereby blocking the first steps in its aggregation process. We also show that squalamine almost completely suppresses the toxicity of α-synuclein oligomers in human neuroblastoma cells by inhibiting their interactions with lipid membranes. We further examine the effects of squalamine in a Caenorhabditis elegans strain overexpressing α-synuclein, observing a dramatic reduction of α-synuclein aggregation and an almost complete elimination of muscle paralysis. These findings suggest that squalamine could be a means of therapeutic intervention in Parkinson’s disease and related conditions.

scholarly journals Inhibition of the SK-N-MC human neuroblastoma cell line in vivo and in vitro by a novel nutrient mixture

2013 ◽  
Vol 29 (5) ◽  
pp. 1714-1720 ◽  
Author(s):  
M. WAHEED ROOMI ◽  
TATIANA KALINOVSKY ◽  
NUSRATH W. ROOMI ◽  
ALEKSANDRA NIEDZWIECKI ◽  
MATTHIAS RATH
Keyword(s):  
Cell Line ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cell Line ◽  
Human Neuroblastoma Cell ◽  
Human Neuroblastoma ◽  
Human Neuroblastoma Cell Line

scholarly journals Neuroinductive properties of mGDNF depend on the producer, E. Coli or human cells

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258289
Author(s):  
Dzhirgala V. Shamadykova ◽  
Dmitry Y. Panteleev ◽  
Nadezhda N. Kust ◽  
Ekaterina A. Savchenko ◽  
Ekaterina Y. Rybalkina ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Ganglion Cells ◽  
Neuroblastoma Cells ◽  
Human Cells ◽  
Hek293 Cells ◽  
Human Neuroblastoma ◽  
Mammalian Expression

The glial cell line‐derived neurotrophic factor (GDNF) is involved in the survival of dopaminergic neurons. Besides, GDNF can also induce axonal growth and creation of new functional synapses. GDNF potential is promising for translation to treat diseases associated with neuronal death: neurodegenerative disorders, ischemic stroke, and cerebral or spinal cord damages. Unproductive clinical trials of GDNF for Parkinson’s disease treatment have induced to study this failure. A reason could be due to irrelevant producer cells that cannot perform the required post-translational modifications. The biological activity of recombinant mGDNF produced by E. coli have been compared with mGDNF produced by human cells HEK293. mGDNF variants were tested with PC12 cells, rat embryonic spinal ganglion cells, and SH-SY5Y human neuroblastoma cells in vitro as well as with a mouse model of the Parkinson’s disease in vivo. Both in vitro and in vivo the best neuro-inductive ability belongs to mGDNF produced by HEK293 cells. Keywords: GDNF, neural differentiation, bacterial and mammalian expression systems, cell cultures, model of Parkinson’s disease.

scholarly journals Ginsenoside Compound K Induces Ros-Mediated Apoptosis and Autophagic Inhibition in Human Neuroblastoma Cells In Vitro and In Vivo

2019 ◽  
Vol 20 (17) ◽  
pp. 4279 ◽  
Author(s):  
Jung-Mi Oh ◽  
Eunhee Kim ◽  
Sungkun Chun
Keyword(s):  
Cell Death ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Autophagic Flux ◽  
Ros Scavenging ◽  
Compound K ◽  
Human Neuroblastoma ◽  
Ginsenoside Compound K

Autophagy can result in cellular adaptation, as well as cell survival or cell death. Modulation of autophagy is increasingly regarded as a promising cancer therapeutic approach. Ginsenoside compound K (CK), an active metabolite of ginsenosides isolated from Panax ginseng C.A. Meyer, has been identified to inhibit growth of cancer cell lines. However, the molecular mechanisms of CK effects on autophagy and neuroblastoma cell death have not yet been investigated. In the present study, CK inhibited neuroblastoma cell proliferation in vitro and in vivo. Treatment by CK also induced the accumulation of sub-G1 population, and caspase-dependent apoptosis in neuroblastoma cells. In addition, CK promotes autophagosome accumulation by inducing early-stage autophagy but inhibits autophagic flux by blocking of autophagosome and lysosome fusion, the step of late-stage autophagy. This effect of CK appears to be mediated through the induction of intracellular reactive oxygen species (ROS) and mitochondria membrane potential loss. Moreover, chloroquine, an autophagy flux inhibitor, further promoted CK-induced apoptosis, mitochondrial ROS induction, and mitochondria damage. Interestingly, those promoted phenomena were rescued by co-treatment with a ROS scavenging agent and an autophagy inducer. Taken together, our findings suggest that ginsenoside CK induced ROS-mediated apoptosis and autophagic flux inhibition, and the combination of CK with chloroquine, a pharmacological inhibitor of autophagy, may be a novel therapeutic potential for the treatment of neuroblastoma.

scholarly journals In vitro and in vivo effects of easily administered, low-toxic retinoid and phenylacetate compounds on human neuroblastoma cells

2003 ◽  
Vol 89 (2) ◽  
pp. 412-419 ◽  
Author(s):  
N Sidell ◽  
M Pasquali ◽  
S Malkapuram ◽  
A B Barua ◽  
T Wanichkul ◽  
...  
Keyword(s):  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma ◽  
Low Toxic ◽  
In Vivo Effects
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