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Disruption of insulin-like growth factor-I expression in type IIalphaI collagen-expressing cells reduces bone length and width in mice.

Authors
Govoni, KE; Lee, SK; Chung, YS; Behringer, RR; Wergedal, JE; Baylink, DJ; Mohan, S
Citation
Physiological genomics, 30(3):354-362, 2007
Journal Title
Physiological genomics
ISSN
1094-83411531-2267
Abstract
It is well established that insulin-like growth factor (IGF)-I is critical for the regulation of peak bone mineral density (BMD) and bone width. However, the role of systemic vs. local IGF-I is not well understood. To determine the role local IGF-I plays in regulating BMD and bone width, we crossed IGF-I flox/flox mice with procollagen, typeIIalphaI-Cre mice to generate conditional mutants in which chondrocyte-derived IGF-I was disrupted. Bone parameters were measured by dual X-ray absorptiometry at 2, 4, 8, and 12 wk of age and peripheral quantitative computed tomography at 12 wk of age. Body length, areal BMD, and bone mineral content (BMC) were reduced (P or = 0.20). In conclusion, IGF-I from cells expressing procollagen type IIalphaI regulates bone accretion that occurs during postnatal growth period.
MeSH terms
AnimalsBone Development/genetics*Bone and Bones/anatomy & histologyBone and Bones/physiologyCollagen Type II/metabolism*FemaleFibroblast Growth Factor 2/geneticsInsulin-Like Growth Factor Binding Proteins/geneticsInsulin-Like Growth Factor I/analysisInsulin-Like Growth Factor I/genetics*MaleMiceMice, Inbred C57BLMice, KnockoutRNA, Messenger/analysis
DOI
10.1152/physiolgenomics.00022.2007
PMID
17519362
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
AJOU Authors
정, 윤석
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