pubmed-article:17279553 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17279553 | lifeskim:mentions | umls-concept:C0025936 | lld:lifeskim |
pubmed-article:17279553 | lifeskim:mentions | umls-concept:C0011304 | lld:lifeskim |
pubmed-article:17279553 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
pubmed-article:17279553 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
pubmed-article:17279553 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:17279553 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:17279553 | pubmed:dateCreated | 2007-2-20 | lld:pubmed |
pubmed-article:17279553 | pubmed:abstractText | Our groups have reported that tumor necrosis factor-alpha (TNF-alpha) causes myelin damage and apoptosis of oligodendrocytes and their precursors in vitro and in vivo. We also have reported that insulin-like growth factor-I (IGF-I) can protect cultured oligodendrocytes and their precursors from TNF-alpha-induced damage. In this study, we investigated whether IGF-I can protect oligodendrocytes and myelination from TNF-alpha-induced damage in vivo by cross-breeding TNF-alpha transgenic (Tg) mice with IGF-I Tg mice that overexpress IGF-I exclusively in brain. At 8 weeks of age, compared with those of wild-type (WT) mice, the brain weights of TNF-alpha Tg mice were decreased by approximately 20%, and those of IGF-I Tg mice were increased by approximately 20%. The brain weights of mice that carry both TNF-alpha and IGF-I transgenes (TNF-alpha/IGF-I Tg mice) did not differ from those of WT mice. As judged by histochemical staining and immunostaining, myelin content in the cerebellum of TNF-alpha/IGF-I Tg mice was similar to that in WT mice and much more than that in TNF-alpha Tg mice. Consistently, Western immunoblot analysis showed that myelin basic protein (MBP) abundance in the cerebellum of TNF-alpha/IGF-I Tg mice was double that in TNF-alpha Tg mice. In comparison with WT mice, the number of oligodendrocytes was decreased by approximately 36% in TNF-alpha Tg mice, whereas it was increased in IGF-I Tg mice by approximately 40%. Oligodendrocyte number in TNF-alpha/IGF-I Tg mice was almost twice that in TNF-alpha Tg mice. Furthermore, IGF-I overexpression significantly reduced TNF-alpha-induced increases in apoptotic cell number, active caspase-3 abundance, and degradaion of MBP. Our results indicate that IGF-I is capable of protecting myelin and oligodendrocytes from TNF-alpha-induced damage in vivo. | lld:pubmed |
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pubmed-article:17279553 | pubmed:language | eng | lld:pubmed |
pubmed-article:17279553 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17279553 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17279553 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17279553 | pubmed:month | Mar | lld:pubmed |
pubmed-article:17279553 | pubmed:issn | 0360-4012 | lld:pubmed |
pubmed-article:17279553 | pubmed:author | pubmed-author:KolliasGeorge... | lld:pubmed |
pubmed-article:17279553 | pubmed:author | pubmed-author:YePingP | lld:pubmed |
pubmed-article:17279553 | pubmed:author | pubmed-author:D'ErcoleA... | lld:pubmed |
pubmed-article:17279553 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17279553 | pubmed:volume | 85 | lld:pubmed |
pubmed-article:17279553 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17279553 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17279553 | pubmed:pagination | 712-22 | lld:pubmed |
pubmed-article:17279553 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17279553 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17279553 | pubmed:articleTitle | Insulin-like growth factor-I ameliorates demyelination induced by tumor necrosis factor-alpha in transgenic mice. | lld:pubmed |
pubmed-article:17279553 | pubmed:affiliation | Division of Endocrinology, Department of Pediatrics, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7039, USA. ping_ye@med.unc.edu | lld:pubmed |
pubmed-article:17279553 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17279553 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:21937 | entrezgene:pubmed | pubmed-article:17279553 | lld:entrezgene |
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