Local Strain Distribution and Increased Intracellular Ca2+ Signaling in Bovine Articular Cartilage Exposed to Compressive Strain.
Local Strain Distribution and Increased Intracellular Ca2+ Signaling in Bovine Articular Cartilage Exposed to Compressive Strain.
复制标题
DOI：
10.1115/1.4045807
复制
发表时间：
2019-12
期刊：
影响因子：
--
通讯作者：
Wenjing Huang;Minami Nagasaka;K. Furukawa;T. Ushida
中科院分区：
文献类型：
--
作者：
Wenjing Huang;Minami Nagasaka;K. Furukawa;T. Ushida
关节软骨在体内生理负荷下暴露于约10%的压缩应变，并且细胞内Ca 2+信号传导是软骨细胞在这种物理刺激下的最早反应之一。然而，它仍然是未知的压缩应变本身是否引起细胞内Ca 2+信号在软骨细胞位于每一层（从表面到深处）在相同的方式与生理水平的应变。因此，本研究的目的是确定局部应变的分布和增加细胞内Ca 2+信号在层依赖性细胞群响应于10%压缩应变负荷。为此，在每层中测量应力松弛曲线以计算层特异性变形特性。此外，使用荧光Ca 2+指示剂Fluo-3记录软骨细胞内Ca 2+信号随时间的层特异性变化，以确定每个深度处Ca 2+信号增加的细胞比例。结果表明，与其他层相比，表层的压缩应变较大。然而，增加的细胞内Ca 2+信号中观察到一个突出的软骨细胞的深层内，但不是表面层，软骨。此外，在深层软骨的软骨细胞首先响应于压缩应变，其次是在中间区的软骨细胞。我们的研究结果表明，在生理压缩水平，刺激和传输的Ca 2+信号在关节软骨是不是简单地定义为局部变形。
Articular cartilage is exposed to compressive strain of approximately 10% under physiological loads in vivo, and intracellular Ca2+ signaling is one of the earliest responses in chondrocytes under this physical stimulation. However, it remains unknown whether compressive strain itself evokes intracellular Ca2+ signaling in chondrocytes located within each layer (from surface to deep) in an equal manner with physiological levels of strain. The purpose of this study, therefore, was to determine the distribution of local strain and increased intracellular Ca2+ signaling in layer-dependent cell populations in response to 10% compressive strain loading. For this purpose, stress-relaxation curves were measured in each layer to calculate layer-specific deformation properties. In addition, layer-specific changes in chondrocyte intracellular Ca2+ signals were recorded over time using a fluorescent Ca2+ indicator, Fluo-3, to establish ratios of cells with increased Ca2+ signaling at each depth. The results showed that the surface layer was compressed with a larger strain compared with other layers. However, increased intracellular Ca2+ signals were observed in a prominent number of chondrocytes within the deep layer, but not the surface layer, of cartilage. Furthermore, chondrocytes in deep-layer cartilage responded first to the compressive strain, followed by chondrocytes in the middle zone. Our results suggest that at a physiological compression level, stimulation and transmission of Ca2+ signaling in articular cartilage is not simply defined by local deformation.