破骨细胞
骨重建
骨吸收
串扰
成骨细胞
细胞生物学
吸收
前列腺素E2
化学
机械转化
内分泌学
压电1
平衡
内科学
生物
医学
生物化学
离子通道
物理
光学
受体
体外
机械敏感通道
作者
Lijun Wang,Xiuling You,Sutada Lotinun,Lingli Zhang,Nan Wu,Weiguo Zou
标识
DOI:10.1038/s41467-019-14146-6
摘要
Abstract Wolff’s law and the Utah Paradigm of skeletal physiology state that bone architecture adapts to mechanical loads. These models predict the existence of a mechanostat that links strain induced by mechanical forces to skeletal remodeling. However, how the mechanostat influences bone remodeling remains elusive. Here, we find that Piezo1 deficiency in osteoblastic cells leads to loss of bone mass and spontaneous fractures with increased bone resorption. Furthermore, Piezo1 -deficient mice are resistant to further bone loss and bone resorption induced by hind limb unloading, demonstrating that PIEZO1 can affect osteoblast-osteoclast crosstalk in response to mechanical forces. At the mechanistic level, in response to mechanical loads, PIEZO1 in osteoblastic cells controls the YAP-dependent expression of type II and IX collagens. In turn, these collagen isoforms regulate osteoclast differentiation. Taken together, our data identify PIEZO1 as the major skeletal mechanosensor that tunes bone homeostasis.
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