Calcium signaling is required for ultrasound-stimulated aggrecan synthesis by rat chondrocytes
Calcium signaling is required for ultrasound-stimulated aggrecan synthesis by rat chondrocytes
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DOI：
10.1016/s0736-0266(01)00069-9
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发表时间：
2002-01-01
影响因子：
2.8
通讯作者：
Bolander, ME
中科院分区：
文献类型：
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作者：
Parvizi, J;Parpura, V;Bolander, ME
低强度超声波加速人类骨折愈合。在大鼠股骨骨折模型中，超声促进愈合与蛋白多糖表达增加相关。在这里，我们报告了超声刺激原代大鼠软骨细胞升高细胞内钙[Ca 2 +]浓度（i.）在较低压力（175-320 kPa）下，[Ca 2 +]（j）的增加是快速和短暂的，但在较高的超声暴露（350-500 kPa）下，[Ca 2 +]（j）的增加是快速和持续的。用1，2-双（2-氨基苯氧基）乙烷-N-N '，N'-四乙酸（BAPTA-AM）螯合线粒体内[Ca ~（2+）]（i），用Thapsigargin阻断Ca ~（2+）/ATP酶诱导的线粒体[Ca ~（2+）]（i）释放，或用EGTA去除培养液中的[Ca ~（2+）]（i），均能抑制超声波对蛋白多糖合成的刺激作用。这些结果表明，与加速骨折愈合相关的细胞基质蛋白聚糖的超声刺激合成是由细胞内钙信号介导的。(C)2002骨科研究学会。由爱思唯尔科技有限公司出版。保留所有权利。
Low-intensity ultrasound accelerates fracture healing in humans. In rat femur fracture models, ultrasound advanced healing is associated with increased proteoglycan expression. Here we report that ultrasound stimulation of primary rat chondrocytes elevated the intracellular concentration of calcium [Ca2+](i.) The [Ca2+](j) increase was rapid and transient at lower pressures (175-320 kPa), but rapid and sustained at higher ultrasound exposures (350-500 kPa). Chelating internal [Ca2+](i) with 1,2-bis(2-aminophenoxy) ethane-N-N-N',N'- tetraacetic acid (BAPTA-AM), stopping the Ca2+/ATP-ase induced mitochondrial release of [Ca2+](i) with Thapsigargin, or removing [Ca2+](i) from the medium with EGTA inhibited the stimulatory effects of ultrasound on proteoglycan synthesis. These results imply that ultrasound-stimulated synthesis of cell matrix proteoglycan, associated with accelerated fracture healing, is mediated by intracellular calcium signaling. (C) 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.