紐約州立大學石溪分校骨科生物工程研究實驗室主任Yi-Xian Qin領導完成的一項研究表明，中等強度的超聲能刺激成骨細胞的流動性，并觸發(fā)其鈣的釋放,，鈣釋放促骨細胞的增長,。該技術可以提供一種方法來開發(fā)非藥物治療骨質疏松癥,、骨折等涉及骨質流失癥狀的疾病,。
像骨骼、肌肉等組織受到機械負荷和應激如運動等刺激后存在強大的動態(tài)平衡狀態(tài),。Qin醫(yī)生和石溪分校的同事Shu Zhang,、Jiqi Cheng正研究成骨細胞是如何應對機械信號如超聲的。
在小鼠細胞實驗模型中,，研究小組創(chuàng)造了一種新的聲輻射力（ARF）的超聲形式,，只適用于一分鐘內單個成骨細胞,。他們一致認為ARF通過聚焦超聲束誘導細胞骨架重排，促進細胞的活力和流動,，加速細胞內鈣離子運輸和濃度,。
Qin醫(yī)生表示該裝置正在開發(fā)作為一種新的診斷工具，可以預測早期骨丟失,。該項研究項目是由國立衛(wèi)生研究院,、國家空間生物醫(yī)學研究所部分資助。（生物谷：Bioon.com）
doi:10.1371/journal.pone.0038343
PMC:
PMID:
Mechanobiological Modulation of Cytoskeleton and Calcium Influx in Osteoblastic Cells by Short-Term Focused Acoustic Radiation Force
Shu Zhang1,2, Jiqi Cheng1, Yi-Xian Qin1*
Mechanotransduction has demonstrated potential for regulating tissue adaptation in vivo and cellular activities in vitro. It is well documented that ultrasound can produce a wide variety of biological effects in biological systems. For example, pulsed ultrasound can be used to noninvasively accelerate the rate of bone fracture healing. Although a wide range of studies has been performed, mechanism for this therapeutic effect on bone healing is currently unknown. To elucidate the mechanism of cellular response to mechanical stimuli induced by pulsed ultrasound radiation, we developed a method to apply focused acoustic radiation force (ARF) (duration, one minute) on osteoblastic MC3T3-E1 cells and observed cellular responses to ARF using a spinning disk confocal microscope. This study demonstrates that the focused ARF induced F-actin cytoskeletal rearrangement in MC3T3-E1 cells. In addition, these cells showed an increase in intracellular calcium concentration following the application of focused ARF. Furthermore, passive bending movement was noted in primary cilium that were treated with focused ARF. Cell viability was not affected. Application of pulsed ultrasound radiation generated only a minimal temperature rise of 0.1°C, and induced a streaming resulting fluid shear stress of 0.186 dyne/cm2, suggesting that hyperthermia and acoustic streaming might not be the main causes of the observed cell responses. In conclusion, these data provide more insight in the interactions between acoustic mechanical stress and osteoblastic cells. This experimental system could serve as basis for further exploration of the mechanosensing mechanism of osteoblasts triggered by ultrasound.
