内科学
内分泌学
成骨细胞
骨保护素
骨钙素
脂联素受体1
碱性磷酸酶
脂联素
转基因小鼠
骨矿物
受体
生物
化学
转基因
骨质疏松症
医学
体外
胰岛素抵抗
生物化学
激活剂(遗传学)
基因
胰岛素
酶
作者
Yanfu Lin,Ching‐Yi Chen,Tai Yuan Chuang,Yuanhua Lin,Hui Yu Liu,Harry J. Mersmann,Shinn‐Chih Wu,Shih‐Torng Ding
出处
期刊:Bone
[Elsevier]
日期:2014-07-01
卷期号:64: 147-154
被引量:55
标识
DOI:10.1016/j.bone.2014.03.051
摘要
Adiponectin and its receptors are expressed in bone marrow-derived osteoblasts. Previous studies in vivo and in vitro have produced controversial results. The purpose of this study was to use porcine adiponectin receptor 1 transgenic mice (pAdipoR1) as a model to evaluate the role of AdipoR1 on bone physiology at different ages. pAdipoR1 transgenic mice had higher bone mineral density than wild-type mice in both genders at 56 weeks of age. The bone volume and trabecular number, measured by micro-computed tomography (μCT) was significantly greater in transgenic than in wild-type female mice at both 8 and 56 weeks of age. ELISA analysis revealed that both serum osteocalcin and osteoprotegerin (OPG) were significantly increased in 8-week old pAdipoR1 transgenic mice of both genders. Furthermore, serum OPG was elevated at 32 and 56 weeks of age in female and male pAdipoR1 transgenic mice. Serum TRAP5b concentration was reduced in 8 and 56 weeks old male pAdipoR1 mice compared with wild-type male mice. Knock-down of AdipoR1 significantly decreased gene expression of osteocalcin, OPG, alkaline phosphatase and msh homeobox 2 and the mineralization in MC3T3-E1 cells and mesenchymal stem cells. In addition, pathscan analysis and real-time PCR analysis suggest AdipoR1 regulates osteoblast differentiation through GSK-3 β and β-Catenin signaling. Consequently, the lack of AdipoR1 impaired osteoblast differentiation and bone formation. We conclude that AdipoR1 is a critical factor for the osteoblast differentiation and bone homeostasis.
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