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APPL1 negatively regulates bone mass, possibly by controlling the fate of bone marrow mesenchymal progenitor cells
Proceedings of the Japan Academy, Series B ( IF 3.1 ) Pub Date : 2020-10-09 , DOI: 10.2183/pjab.96.027
Yuan-Yu LIN, Lily Q. DONG

Adiponectin is an adipokine that can exert a regulatory function on bone metabolism. However, there are many contradictions between clinical and pre-clinical studies on adiponectin. APPL1 is an adaptor protein that can interact with adiponectin receptors. In the current study, we found that knockout of the Appl1 gene in male mice was associated with higher bone volume and numbers of trabeculae than in females or controls. The trabecular thickness, cortical thickness, ratio of bone volume/trabecular volume, cross-sectional bone area, and mean polar moment of inertia increased in Appl1 KO mice compared with wild-type mice. The number of osteoblasts increased but the number of adipocytes decreased in Appl1 KO mice. Knockdown of Appl1 impaired adipogenesis in bone marrow-derived mesenchymal stem cells. Mineralization was increased by knockdown of Appl1 during osteoblast differentiation. Data from differentiation-related genes showed results consistent with the in vivo effects. In summary, this study provides further clarification of the effect of the adiponectin signaling pathway on bone metabolism.



中文翻译:

APPL1可能通过控制骨髓间充质祖细胞的命运来负面调节骨量

脂联素是一种可以对骨代谢发挥调节作用的脂肪因子。但是,脂联素的临床研究和临床前研究之间存在许多矛盾。APPL1是可以与脂联素受体相互作用的衔接蛋白。在当前的研究中,我们发现,与雌性或对照组相比,雄性小鼠中Appl1基因的敲除与更高的骨量和小梁数量有关。与野生型小鼠相比,Appl1 KO小鼠的骨小梁厚度,皮质厚度,骨体积/骨小梁体积之比,横截面骨面积和平均惯性矩增加。Appl1 KO小鼠的成骨细胞数量增加,但脂肪细胞数量减少。击倒Appl1骨髓间充质干细胞的脂肪形成受损。成骨细胞分化期间通过敲除Appl1可以增加矿化作用。来自分化相关基因的数据显示出与体内效应一致的结果。总之,这项研究进一步阐明了脂联素信号传导途径对骨代谢的影响。

更新日期:2020-10-28
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