| pubmed-article:8632765 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C1704256 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C0235032 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C1515406 | lld:lifeskim |
| pubmed-article:8632765 | lifeskim:mentions | umls-concept:C2353566 | lld:lifeskim |
| pubmed-article:8632765 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8632765 | pubmed:dateCreated | 1996-7-3 | lld:pubmed |
| pubmed-article:8632765 | pubmed:abstractText | Neurodegeneration associated with Alzheimer's disease is believed to involve toxicity to beta-amyloid (A beta) and related peptides. Treatment of cultured rat hippocampal neurons with A beta 1-40 (1 microM) or the active fragment A beta 25-35 (1 microM) for 5 days led to a approximately 40-50% decrease in neuronal viability. The hydrophilic antioxidant ascorbic acid (300 microM) and the lipophilic antioxidant 2-mercaptoethanol (10 microM) both protected significantly against A beta neurotoxicity. Despite the protective effects of these antioxidants, both acute and chronic treatments with A beta 25-35 did not increase production of superoxide anions, as monitored with the fluorescent probe hydroethidine. Similarly, overexpression of Cu/Zn-superoxide dismutase using adenovirus-mediated gene transfer did not protect against A beta neurotoxicity. A beta neurotoxicity, however, was prevented in cultures infected with a recombinant, replication-defective adenovirus overexpressing the Ca2+ binding protein calbindin D28k. Transforming growth factor-beta 1 (TGF-beta 1) has been shown to protect neurons against both Ca(2+)- and free radical-mediated neuronal degeneration. We found that A beta neurotoxicity was significantly attenuated by single treatments with TGF-beta 1 (0.1-10 ng/ml) and prevented by repetitive treatments (10 ng/ml/day). The protective effects of TGF-beta 1 were associated with a preservation of mitochondrial potential and function, as determined with rhodamine-123-based microfluorimetry. Because both increased oxidative stress and pathophysiological Ca2+ fluxes can impair mitochondrial function, preservation of mitochondrial potential by TGF-beta 1 could be directly associated with its protection against A beta neurotoxicity. The ability of TGF-beta 1 to increase the expression of the anti-apoptotic proteins Bcl-2 and Bcl-XL is discussed in this context. | lld:pubmed |
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| pubmed-article:8632765 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8632765 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8632765 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8632765 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8632765 | pubmed:issn | 0026-895X | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:ReedJ CJC | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:MillerR JRJ | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:KrajewskiSS | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:RoosR PRP | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:ThompsonC BCB | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:GhadgeG DGD | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:BoiseL HLH | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:PrehnJ HJH | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:BindokasV PVP | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:JordánJJ | lld:pubmed |
| pubmed-article:8632765 | pubmed:author | pubmed-author:GalindoM FMF | lld:pubmed |
| pubmed-article:8632765 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8632765 | pubmed:volume | 49 | lld:pubmed |
| pubmed-article:8632765 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8632765 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8632765 | pubmed:pagination | 319-28 | lld:pubmed |
| pubmed-article:8632765 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:8632765 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8632765 | pubmed:articleTitle | Protective effect of transforming growth factor-beta 1 on beta-amyloid neurotoxicity in rat hippocampal neurons. | lld:pubmed |
| pubmed-article:8632765 | pubmed:affiliation | Department of Pharmacological and Physiological Sciences, University of Chicago, Illinois 60637, USA. | lld:pubmed |
| pubmed-article:8632765 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8632765 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8632765 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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