1
40
2
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s11064-011-0591-2" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11064-011-0591-2</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
134-142
Issue
1
Volume
37
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Differential Effect Of Nimodipine In Attenuating Iron-induced Toxicity In Brain- And Blood-brain Barrier-associated Cell Types
Publisher
An entity responsible for making the resource available
Neurochemical Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
Astrocytes; Biochemistry & Molecular Biology; central-nervous-system; cerebrospinal-fluid; cultured astrocytes; intracerebral hemorrhage; Iron in brain; Metal toxicity; Neurodegenerative diseases; neurodegenerative disorders; neurons; Neurosciences & Neurology; Nimodipine; oxidative; parkinsons-disease; redox-active iron; stress; substantia-nigra; transferrin receptor; Vascular endothelial cells
Creator
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Lockman J A; Geldenhuys W J; Bohn K A; DeSilva S F; Allen D D; Van der Schyf C J
Description
An account of the resource
Metal homeostasis is increasingly being evaluated as a therapeutic target in stroke and neurodegenerative diseases. Metal dysregulation has been shown to lead to protein aggregation, plaque formation and neuronal death. In 2007, we first reported that voltage-gated calcium channels act as a facile conduit for the entry of free ferrous (Fe2+) ions into neurons. Herein, we evaluate differential iron toxicity to central nervous system cells and assess the ability of the typical L-type voltage-gated calcium channel blocker nimodipine to attenuate iron-induced toxicity. The data demonstrate that iron sulfate induces a dose-dependent decrease in cell viability in rat brain endothelial cells (RBE4; LC50 = 150 mu M), neuronal cells (Neuro-2 alpha neuroblastoma; LC50 = 400 mu M), and in astrocytes (DI TNC1; LC50 = 1.1 mM). Pre-treatment with nimodipine prior to iron sulfate exposure provided a significant (P < 0.05) increase in viable cell numbers for RBE4 (2.5-fold), Neuro2-alpha (similar to 2-fold), and nearly abolished toxicity in primary neurons. Astrocytes were highly resistant to iron toxicity compared to the other cell types tested and nimodipine had no (P > 0.05) protective effect in these cells. The data demonstrate variable susceptibility to iron overload conditions in different cell types of the brain and suggest that typical L-type voltage-gated calcium channel blockers (here represented by nimodipine), may serve as protective agents in conditions involving iron overload, particularly in cell types highly susceptible to iron toxicity.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s11064-011-0591-2" target="_blank" rel="noreferrer noopener">10.1007/s11064-011-0591-2</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Allen D D
Astrocytes
Biochemistry & Molecular Biology
Bohn K A
central-nervous-system
cerebrospinal-fluid
cultured astrocytes
DeSilva S F
Geldenhuys W J
intracerebral hemorrhage
Iron in brain
Journal Article or Conference Abstract Publication
Lockman J A
Metal toxicity
Neurochemical Research
Neurodegenerative Diseases
neurodegenerative disorders
Neurons
Neurosciences & Neurology
nimodipine
oxidative
parkinsons-disease
redox-active iron
Stress
substantia-nigra
transferrin receptor
Van der Schyf C J
Vascular endothelial cells
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.brainres.2012.10.029" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.brainres.2012.10.029</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
133-139
Volume
1489
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Ngp1-01, A Multi-targeted Polycyclic Cage Amine, Attenuates Brain Endothelial Cell Death In Iron Overload Conditions
Publisher
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Brain Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-12
Subject
The topic of the resource
activator; barrier; calcium channels; channels provide; intracerebral hemorrhage; Iron-overload; neurodegeneration; neurodegenerative disorders; neuroprotection; Neurosciences & Neurology; Nimodipine; parkinsons-disease; permeability; rat-brain; toxicity; transport; Vascular endothelial cells; Voltage-gated calcium channel
Creator
An entity primarily responsible for making the resource
Lockman J A; Geldenhuys W J; Jones-Higgins M R; Patrick J D; Allen D D; Van der Schyf C J
Description
An account of the resource
Development and progression of neurodegenerative disorders have, amongst other potential causes, been attributed to a disruption of iron regulatory mechanisms and iron accumulation. Excess extracellular iron may enter cells via nontraditional routes such as voltage-gated calcium channels and N-methyl-D-aspartate (NMDA) receptors leading to intracellular oxidative damage and ultimately mitochondrial failure. Nimodipine, an L-type calcium channel blocker has been shown to reduce iron-induced toxicity in neuronal and brain endothelial cells. Our current study investigates NGP1-01, a multimodal drug acting as an antagonist at both the NMDA receptor and the L-type calcium channel. Our previous studies support NGP1-01. as a promising neuroprotective agent in diseases involving calcium-related excitotoxicity. We demonstrate here that NGP1-01 (1 and 10 mu M) pretreatment abrogates the effects of iron overload in brain endothelial cells protecting cellular viability. Both concentrations of NGP1-01 were found to attenuate iron-induced reduction in cellular viability to a similar extent, and were statistically significant. To further verify the mechanism, the L-type calcium channel agonist FPL 64176 was administered to promote iron uptake. Addition of NGP1-01 dose-dependently reduced FPL 64176 stimulated uptake of iron. These data support further evaluation of NGP1-01 as a neuroprotective agent, not only in diseases associated with excitotoxicity, but also in those of iron overload. (C) 2012 Elsevier B.V. All rights reserved.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.brainres.2012.10.029" target="_blank" rel="noreferrer noopener">10.1016/j.brainres.2012.10.029</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
activator
Allen D D
barrier
Brain research
Calcium Channels
channels provide
Geldenhuys W J
intracerebral hemorrhage
Iron-overload
Jones-Higgins M R
Journal Article or Conference Abstract Publication
Lockman J A
Neurodegeneration
neurodegenerative disorders
Neuroprotection
Neurosciences & Neurology
nimodipine
parkinsons-disease
Patrick J D
Permeability
rat-brain
toxicity
transport
Van der Schyf C J
Vascular endothelial cells
Voltage-gated calcium channel