ArticleBritish journal of pharmacology2015
Prevention of the degeneration of human dopaminergic neurons in an astrocyte co-culture system allowing endogenous drug metabolism.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 58 citations in OpenAlex.
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- Co-Culture Models: Key Players in In Vitro Neurotoxicity, Neurodegeneration and BBB Modeling Studies.Biomedicines · 2024Review
- Identification of the bacterial metabolite aerugine as potential trigger of human dopaminergic neurodegeneration.Environment international · 2023Article
- Probabilistic cell seeding and non-autofluorescent 3D-printed structures as scalable approach for multi-level co-culture modeling.Materials today. Bio · 2023Article
- Neurotoxicity and underlying cellular changes of 21 mitochondrial respiratory chain inhibitors.Archives of toxicology · 2021Article
- The Role of Astrocytes in the Neurorepair Process.Frontiers in cell and developmental biology · 2021Article
- Design and evaluation of bi-functional iron chelators for protection of dopaminergic neurons from toxicants.Archives of toxicology · 2020Article
- Preparation and Neuroprotective Activity of Glucuronomannan Oligosaccharides in an MPTP-Induced Parkinson's Model.Marine drugs · 2020Article
- A primary neural cell culture model to study neuron, astrocyte, and microglia interactions in neuroinflammation.Journal of neuroinflammation · 2020Article
- Roflupram exerts neuroprotection via activation of CREB/PGC-1α signalling in experimental models of Parkinson's disease.British journal of pharmacology · 2020Article
- Enhanced differentiation of human dopaminergic neuronal cell model for preclinical translational research in Parkinson's disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Neurotoxicity of pesticides.Acta neuropathologica · 2019Review
- Development of a neurotoxicity assay that is tuned to detect mitochondrial toxicants.Archives of toxicology · 2019Article
- Major changes of cell function and toxicant sensitivity in cultured cells undergoing mild, quasi-natural genetic drift.Archives of toxicology · 2018Article
- Prevention of neuronal apoptosis by astrocytes through thiol-mediated stress response modulation and accelerated recovery from proteotoxic stress.Cell death and differentiation · 2018Article
- Neuroprotective effects of the gliopeptide ODN in an in vivo model of Parkinson's disease.Cellular and molecular life sciences : CMLS · 2018Article
- Article
- An adverse outcome pathway for parkinsonian motor deficits associated with mitochondrial complex I inhibition.Archives of toxicology · 2018Review
- 3D Differentiation of LUHMES Cell Line to Study Recovery and Delayed Neurotoxic Effects.Current protocols in toxicology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeFew neuropharmacological model systems use human neurons. Moreover, available test systems rarely reflect functional roles of co-cultured glial cells. There is no human in vitro counterpart of the widely used 1-methyl-4-phenyl-tetrahydropyridine (MPTP) mouse model of Parkinson's disease EXPERIMENTAL APPROACH: We generated such a model by growing an intricate network of human dopaminergic neurons on a dense layer of astrocytes. In these co-cultures, MPTP was metabolized to 1-methyl-4-phenyl-pyridinium (MPP(+) ) by the glial cells, and the toxic metabolite was taken up through the dopamine transporter into neurons. Cell viability was measured biochemically and by quantitative neurite imaging, siRNA techniques were also used. KEY
resultsWe initially characterized the activation of PARP. As in mouse models, MPTP exposure induced (poly-ADP-ribose) synthesis and neurodegeneration was blocked by PARP inhibitors. Several different putative neuroprotectants were then compared in mono-cultures and co-cultures. Rho kinase inhibitors worked in both models; CEP1347, ascorbic acid or a caspase inhibitor protected mono-cultures from MPP(+) toxicity, but did not protect co-cultures, when used alone or in combination. Application of GSSG prevented degeneration in co-cultures, but not in mono-cultures. The surprisingly different pharmacological profiles of the models suggest that the presence of glial cells, and the in situ generation of the toxic metabolite MPP(+) within the layered cultures played an important role in neuroprotection. CONCLUSIONS AND IMPLICATIONS: Our new model system is a closer model of human brain tissue than conventional cultures. Its use for screening of candidate neuroprotectants may increase the predictiveness of a test battery.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.