Mechanotransduction has demonstrated potentials for tissue adaptation in vivo and in vitro. It is well documented that ultrasound, as a mechanical signal, can produce a wide variety of biological effects in vitro and in vivo[1]. For example, pulsed ultrasound can be used to accelerate the rate of bone fracture healing noninvasively. Although a wide range of studies have been done, mechanism for this therapeutic effect on bone healing is currently unknown and still under active investigation. In our previous studies, we have developed methodology allowed in vitro manipulating osteoblastic cells using acoustic radiation force (ARF) generated by ultrasound without the effects of acoustic streaming and ultrasound-induced temperature rise. Furthermore, we also confirmed that ARF modulated intracellular Ca2+ transient in MC3T3-E1 osteoblast-like cells in a strain and frequency-dependent manner. A potential mechanism by which bone cells may sense ultrasound is through their structures such as primary cilia and cytoskeletons. The purpose of the current study was to evaluate the hypothesis that acoustic radiation force can regulate the activities of the primary cilium and the cytoskeleton of the cells, which act as the mechanotransductive signals to mediate Ca2+ flux, as a pathway in response to cyclic loading.

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