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Adiponectin receptor 1 involves in regulating bone formation and osteoblast differentiation
Author(s) -
Lin Yuan-Yu,
Wu Shinn-Chih,
Liu Bing-Hsun,
Chen Ching-Yi,
Mersmann Harry John,
Ding Shih-Torng
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.693.7
Subject(s) - osteoblast , medicine , endocrinology , adiponectin receptor 1 , osteocalcin , mesenchymal stem cell , adiponectin , progenitor cell , osteoporosis , chemistry , bone marrow , microbiology and biotechnology , biology , stem cell , in vitro , alkaline phosphatase , biochemistry , insulin resistance , insulin , enzyme
Osteoblasts and adipocytes can derive from the same progenitor cells in bone marrow. The proportion of osteoblasts and adipocytes are associated with age‐related osteoporosis. To evaluate the roles of adiponectin and its receptor (AdipoR1) in regulating the cell fate between adipocytes and osteoblasts, we used the AdipoR1 transgenic and wild type mice to establish mesenchymal stem cells (MSCs) for in vitro study and the bone physiological relevance of the mice were analyzed by micro‐CT analysis. The bone traits of percent bone volume, trabecular number and trabecular thickness were significantly higher in AdipoR1 transgenic mice compared with wild type mice that have the same pattern of serum osteocalcin (bone formation marker) concentration. During differentiation of osteoblasts, the mRNA expression of msh homeobox 2 gene, a key transcription factor of osteoblast differentiation, of AdipoR1‐tMSCs were greater than that of wild type MSCs. Furthermore, paraffin embedding sections of femur has less trap‐positive staining cells in AdipoR1 transgenic mice. These data suggest that the adiponectin may promote osteogenesis and inhibit osteoclastogenesis through its receptor, AdipoR1. Understanding of such mechanism will facilitate the development of treatments for metabolic‐linked bone diseases.