| pubmed-article:12019317 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12019317 | lifeskim:mentions | umls-concept:C0011065 | lld:lifeskim |
| pubmed-article:12019317 | lifeskim:mentions | umls-concept:C0035316 | lld:lifeskim |
| pubmed-article:12019317 | lifeskim:mentions | umls-concept:C1517499 | lld:lifeskim |
| pubmed-article:12019317 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:12019317 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:12019317 | pubmed:dateCreated | 2002-5-20 | lld:pubmed |
| pubmed-article:12019317 | pubmed:abstractText | Injury-induced downregulation of neurotrophin receptors may limit the response of neurons to trophic factors, compromising their ability to survive. We tested this hypothesis in a model of CNS injury: retinal ganglion cell (RGC) death after transection of the adult rat optic nerve. TrkB mRNA rapidly decreased in axotomized RGCs to approximately 50% of the level in intact retinas. TrkB gene transfer into RGCs combined with exogenous BDNF administration markedly increased neuronal survival: 76% of RGCs remained alive at 2 weeks after axotomy, a time when >90% of these neurons are lost without treatment. Activation of mitogen-activated protein kinase, but not phosphatidylinositol-3 kinase, was required for TrkB-induced survival. These data provide proof-of-principle that enhancing the capacity of injured neurons to respond to trophic factors can be an effective neuroprotective strategy in the adult CNS. | lld:pubmed |
| pubmed-article:12019317 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12019317 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12019317 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12019317 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12019317 | pubmed:month | May | lld:pubmed |
| pubmed-article:12019317 | pubmed:issn | 1529-2401 | lld:pubmed |
| pubmed-article:12019317 | pubmed:author | pubmed-author:ChengLiL | lld:pubmed |
| pubmed-article:12019317 | pubmed:author | pubmed-author:HauswirthWill... | lld:pubmed |
| pubmed-article:12019317 | pubmed:author | pubmed-author:SapiehaPrzemy... | lld:pubmed |
| pubmed-article:12019317 | pubmed:author | pubmed-author:KittlerovaPav... | lld:pubmed |
| pubmed-article:12019317 | pubmed:author | pubmed-author:Di... | lld:pubmed |
| pubmed-article:12019317 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12019317 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12019317 | pubmed:volume | 22 | lld:pubmed |
| pubmed-article:12019317 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12019317 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12019317 | pubmed:pagination | 3977-86 | lld:pubmed |
| pubmed-article:12019317 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12019317 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12019317 | pubmed:articleTitle | TrkB gene transfer protects retinal ganglion cells from axotomy-induced death in vivo. | lld:pubmed |
| pubmed-article:12019317 | pubmed:affiliation | Department of Pathology and Cell Biology, Université de Montréal, Montreal, Quebec H3T 1J4, Canada. | lld:pubmed |
| pubmed-article:12019317 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12019317 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12019317 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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