| pubmed-article:17402968 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0086045 | lld:lifeskim |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0017817 | lld:lifeskim |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0532371 | lld:lifeskim |
| pubmed-article:17402968 | lifeskim:mentions | umls-concept:C0311404 | lld:lifeskim |
| pubmed-article:17402968 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:17402968 | pubmed:dateCreated | 2007-4-3 | lld:pubmed |
| pubmed-article:17402968 | 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. | lld:pubmed |
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| pubmed-article:17402968 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17402968 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17402968 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17402968 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17402968 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:17402968 | pubmed:issn | 0022-3042 | lld:pubmed |
| pubmed-article:17402968 | pubmed:author | pubmed-author:RussellJames... | lld:pubmed |
| pubmed-article:17402968 | pubmed:author | pubmed-author:Berent-Spills... | lld:pubmed |
| pubmed-article:17402968 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17402968 | pubmed:volume | 101 | lld:pubmed |
| pubmed-article:17402968 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17402968 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17402968 | pubmed:pagination | 342-54 | lld:pubmed |
| pubmed-article:17402968 | pubmed:dateRevised | 2007-12-3 | lld:pubmed |
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| pubmed-article:17402968 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17402968 | pubmed:articleTitle | Metabotropic glutamate receptor 3 protects neurons from glucose-induced oxidative injury by increasing intracellular glutathione concentration. | lld:pubmed |
| pubmed-article:17402968 | pubmed:affiliation | Neuroscience Program, University of Michigan, Ann Arbor, Michigan, USA. | lld:pubmed |
| pubmed-article:17402968 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17402968 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:17402968 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17402968 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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