Source:http://linkedlifedata.com/resource/pubmed/id/20926579
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2010-11-24
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pubmed:abstractText |
Animal studies have shown that IGF-I is essential for mammary gland development. Previous studies have suggested that local IGF-I rather than circulating IGF-I is the major mediator of mammary gland development. In the present study we used the hepatic IGF-I transgenic (HIT) and IGF-I knockout/HIT (KO-HIT) mouse models to examine the effects of enhanced circulating IGF-I on mammary development in the presence and absence of local IGF-I. HIT mice express the rat IGF-I transgene under the transthyretin promoter in the liver and have elevated circulating IGF-I and normal tissue IGF-I levels. The KO-HIT mice have no tissue IGF-I and increased circulating IGF-I. Analysis of mammary gland development reveals a greater degree of complexity in HIT mice as compared to control and KO-HIT mice, which demonstrate similar degrees of mammary gland complexity. Immunohistochemical evaluation of glands of HIT mice also suggests an enhanced degree of proliferation of the mammary gland, whereas KO-HIT mice exhibit mammary gland proliferation similar to control mice. In addition, HIT mice have a higher percentage of proliferating myoepithelial and luminal cells than control mice, whereas KO-HIT mice have an equivalent percentage of proliferating myoepithelial and luminal cells as control mice. Thus, our findings show that elevated circulating IGF-I levels are sufficient to promote normal pubertal mammary epithelial development. However, HIT mice demonstrate more pronounced mammary gland development when compared to control and KO-HIT mice. This suggests that both local and endocrine IGF-I play roles in mammary gland development and that elevated circulating IGF-I accelerates mammary epithelial proliferation.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1945-7170
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
151
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5751-61
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pubmed:meshHeading |
pubmed-meshheading:20926579-Aging,
pubmed-meshheading:20926579-Animals,
pubmed-meshheading:20926579-Cell Proliferation,
pubmed-meshheading:20926579-Epithelial Cells,
pubmed-meshheading:20926579-Female,
pubmed-meshheading:20926579-Gene Expression Regulation, Developmental,
pubmed-meshheading:20926579-Insulin-Like Growth Factor I,
pubmed-meshheading:20926579-Mammary Glands, Animal,
pubmed-meshheading:20926579-Mice,
pubmed-meshheading:20926579-Mice, Knockout,
pubmed-meshheading:20926579-Mice, Transgenic,
pubmed-meshheading:20926579-Organ Size,
pubmed-meshheading:20926579-Phosphorylation,
pubmed-meshheading:20926579-Rats,
pubmed-meshheading:20926579-Weight Gain
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pubmed:year |
2010
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pubmed:articleTitle |
Elevated circulating IGF-I promotes mammary gland development and proliferation.
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pubmed:affiliation |
Division of Endocrinology, Diabetes, and Bone Diseases, The Samuel Bronfman Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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