Linked Life Data

17402968

Source:http://linkedlifedata.com/resource/pubmed/id/17402968

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-4-3
pubmed:abstractText
High glucose concentrations cause oxidative injury and programmed cell death in neurons, and can lead to diabetic neuropathy. Activating the type 3 metabotropic glutamate receptor (mGluR3) prevents glucose-induced oxidative injury in dorsal root ganglion neurons co-cultured with Schwann cells. To determine the mechanisms of protection, studies were performed in rat dorsal root ganglion neuron-Schwann cell co-cultures. The mGluR3 agonist 2R,4R-4-aminopyrrolidine-2,4-dicarboxylate prevented glucose-induced inner mitochondrial membrane depolarization, reactive oxygen species accumulation, and programmed cell death, and increased glutathione (GSH) concentration in co-cultured neurons and Schwann cells, but not in neurons cultured without Schwann cells. Protection was diminished in neurons treated with the GSH synthesis inhibitor l-buthionine-sulfoximine, suggesting that mGluR-mediated protection requires GSH synthesis. GSH precursors and the GSH precursor GSH-ethyl ester also protected neurons from glucose-induced injury, indicating that GSH synthesis in Schwann cells, and transport of reaction precursors to neurons, may underlie mGluR-mediated neuroprotection. These results support the conclusions that activating glial mGluR3 protects neurons from glucose-induced oxidative injury by increasing free radical scavenging and stabilizing mitochondrial function, through increased GSH antioxidant defense.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
342-54
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed-meshheading:17402968-Animals, pubmed-meshheading:17402968-Antimetabolites, pubmed-meshheading:17402968-Apoptosis, pubmed-meshheading:17402968-Buthionine Sulfoximine, pubmed-meshheading:17402968-Cells, Cultured, pubmed-meshheading:17402968-Coculture Techniques, pubmed-meshheading:17402968-Diabetic Neuropathies, pubmed-meshheading:17402968-Excitatory Amino Acid Agonists, pubmed-meshheading:17402968-Ganglia, Spinal, pubmed-meshheading:17402968-Glucose, pubmed-meshheading:17402968-Glutathione, pubmed-meshheading:17402968-Hyperglycemia, pubmed-meshheading:17402968-Intracellular Space, pubmed-meshheading:17402968-Mitochondrial Membranes, pubmed-meshheading:17402968-Neurons, Afferent, pubmed-meshheading:17402968-Oxidative Stress, pubmed-meshheading:17402968-Rats, pubmed-meshheading:17402968-Rats, Sprague-Dawley, pubmed-meshheading:17402968-Reactive Oxygen Species, pubmed-meshheading:17402968-Receptors, Metabotropic Glutamate, pubmed-meshheading:17402968-Schwann Cells, pubmed-meshheading:17402968-Up-Regulation
pubmed:year
2007
pubmed:articleTitle
Metabotropic glutamate receptor 3 protects neurons from glucose-induced oxidative injury by increasing intracellular glutathione concentration.
pubmed:affiliation
Neuroscience Program, University of Michigan, Ann Arbor, Michigan, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural