Abstract
Chondromodulin I (ChM-I) was supposed from its limited expression in cartilage and its functions in cultured chondrocytes as a major regulator in cartilage development. Here, we generated mice deficient in ChM-I by targeted disruption of the ChM-I gene. No overt abnormality was detected in endochondral bone formation during embryogenesis and cartilage development during growth stages of ChM-I(-/-) mice. However, a significant increase in bone mineral density with lowered bone resorption with respect to formation was unexpectedly found in adult ChM-I(-/-) mice. Thus, the present study established that ChM-I is a bone remodeling factor.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alleles
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Animals
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Animals, Newborn
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Blotting, Northern
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Blotting, Southern
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Blotting, Western
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Bone Development
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Bone Marrow Cells / metabolism
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Cartilage / embryology
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Cells, Cultured
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Female
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Homozygote
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Intercellular Signaling Peptides and Proteins / genetics*
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Intercellular Signaling Peptides and Proteins / physiology*
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Macrophages / metabolism
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Male
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Membrane Proteins*
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Models, Genetic
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Osteoblasts / metabolism
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RNA, Messenger / metabolism
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Recombination, Genetic
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Reverse Transcriptase Polymerase Chain Reaction
Substances
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Cnmd protein, mouse
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Intercellular Signaling Peptides and Proteins
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Membrane Proteins
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RNA, Messenger