Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice

作者: Tianshun Xu , Paolo Bianco , Larry W. Fisher , Glenn Longenecker , Erica Smith

DOI: 10.1038/1746

关键词:

摘要: The resilience and strength of bone is due to the orderly mineralization a specialized extracellular matrix (ECM) composed type I collagen (90%) host non-collagenous proteins that are, in general, also found other tissues. Biglycan (encoded by gene Bgn) an ECM proteoglycan enriched non-skeletal connective In vitro studies indicate Bgn may function tissue metabolism binding fibrils TGF-beta (refs 5,6), promote neuronal survival. To study role vivo, we generated Bgn-deficient mice. Although apparently normal at birth, these mice display phenotype characterized reduced growth rate decreased mass absence Bgn. our knowledge, this first report which deficiency protein leads skeletal marked low becomes more obvious with age. These serve as animal model osteoporosis.

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