Source:http://linkedlifedata.com/resource/pubmed/id/17008389
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2006-12-20
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| pubmed:abstractText |
This study tested whether elevated levels of IGF-II in the postnatal period can rescue the dwarfism in IGF-I-deficient mice. Heterozygous Igf1 mutant mice [I(+/-) II(wt)] were crossed with heterozygous Igf1 mutant, phosphoenolpyruvate carboxykinase promoter IGF-II transgenic mice [I(+/-) II(tg)], and [I(+/+) II(wt)], [I(+/+) II(tg)], [I(-/-) II(wt)], and [I(-/-) II(tg)] offspring were investigated. IGF-II levels were 11- and 6-fold higher in male and female [I(-/-) II(tg)] vs. [I(-/-) II(wt)] animals. Western ligand blot analysis revealed markedly reduced activities of 30- and 32-kDa IGF binding proteins (IGFBPs) (most likely IGFBP-1 and IGFBP-2) and the 39- to 43-kDa IGFBP-3 double band in serum from IGF-I-deficient mice. These binding proteins were partially restored by overexpression of IGF-II. Analysis of weight data from the early postnatal period until d 60 showed that, in the absence of IGF-I, elevated levels of IGF-II have no effect on body weight gain. A detailed analysis of body proportions, bone parameters, and organ weights of 60-d-old mice also failed to show effects of IGF-II with one important exception: in Igf1 mutant and also Igf1 intact male mice, IGF-II overexpression significantly increased absolute (+32.4 and +28.6%; P < 0.01) and relative kidney weights (+29.0 and +22.4%; P < 0.001). These changes in kidney weight were associated with reduced phosphorylation of p38 MAPK. In summary, our genetic model shows that substantial amounts of IGF-II in the circulation do not rescue the postnatal growth deficit of IGF-I-deficient mice but increase absolute and relative kidney weights of normal and IGF-I-deficient male mice, suggesting a gender-specific role of IGF-II for kidney growth.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding...,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor II,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0013-7227
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
148
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
441-51
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:17008389-Animals,
pubmed-meshheading:17008389-Animals, Outbred Strains,
pubmed-meshheading:17008389-Body Size,
pubmed-meshheading:17008389-Body Weight,
pubmed-meshheading:17008389-Dwarfism,
pubmed-meshheading:17008389-Female,
pubmed-meshheading:17008389-Heterozygote,
pubmed-meshheading:17008389-Insulin-Like Growth Factor Binding Proteins,
pubmed-meshheading:17008389-Insulin-Like Growth Factor I,
pubmed-meshheading:17008389-Insulin-Like Growth Factor II,
pubmed-meshheading:17008389-Kidney,
pubmed-meshheading:17008389-Male,
pubmed-meshheading:17008389-Mice,
pubmed-meshheading:17008389-Mice, Transgenic,
pubmed-meshheading:17008389-Organ Size,
pubmed-meshheading:17008389-Phenotype,
pubmed-meshheading:17008389-Phosphorylation,
pubmed-meshheading:17008389-Pregnancy,
pubmed-meshheading:17008389-Sex Characteristics,
pubmed-meshheading:17008389-Signal Transduction,
pubmed-meshheading:17008389-Transgenes,
pubmed-meshheading:17008389-p38 Mitogen-Activated Protein Kinases
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| pubmed:year |
2007
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| pubmed:articleTitle |
Postnatally elevated levels of insulin-like growth factor (IGF)-II fail to rescue the dwarfism of IGF-I-deficient mice except kidney weight.
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| pubmed:affiliation |
Institute of Molecular Animal Breeding and Biotechnology, Gene Center, University of Munich, D-81377 Munich, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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