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首页> 外文期刊>Osteoarthritis and cartilage >Chondrocyte mechanotransduction: effects of compression on deformation of intracellular organelles and relevance to cellular biosynthesis.
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Chondrocyte mechanotransduction: effects of compression on deformation of intracellular organelles and relevance to cellular biosynthesis.

机译：软骨细胞机械转导：压缩对细胞内细胞器变形的影响以及与细胞生物合成的相关性。

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OBJECTIVE: The effects of mechanical deformation of intact cartilage tissue on chondrocyte biosynthesis in situ have been well documented, but the mechanotransduction pathways that regulate such phenomena have not been elucidated completely. The goal of this study was to examine the effects of tissue deformation on the morphology of a range of intracellular organelles which play a major role in cell biosynthesis and metabolism. DESIGN: Using chemical fixation, high pressure freezing, and electron microscopy, we imaged chondrocytes within mechanically compressed cartilage explants at high magnification and quantitatively and qualitatively assessed changes in organelle volume and shape caused by graded levels of loading. RESULTS: Compression of the tissue caused a concomitant reduction in the volume of the extracellular matrix (ECM), chondrocyte, nucleus, rough endoplasmic reticulum, and mitochondria. Interestingly, however, the Golgi apparatus was able to resist loss of intraorganelle water and retain aportion of its volume relative to the remainder of the cell. These combined results suggest that a balance between intracellular mechanical and osmotic gradients govern the changes in shape and volume of the organelles as the tissue is compressed. CONCLUSIONS: Our results lead to the interpretive hypothesis that organelle volume changes appear to be driven mainly by osmotic interactions while shape changes are mediated by structural factors, such as cytoskeletal interactions that may be linked to extracellular matrix deformations. The observed volume and shape changes of the chondrocyte organelles and the differential behavior between organelles during tissue compression provide evidence for an important mechanotransduction pathway linking translational and post-translational events (e.g., elongation and sulfation of glycosaminoglycans (GAGs) in the Golgi) to cell deformation.
机译：目的：完整的软骨组织的机械变形对软骨细胞原位合成的影响已有充分的文献记载，但调节这种现象的机械传导途径尚未完全阐明。这项研究的目的是研究组织变形对一系列细胞内细胞器的形态的影响，这些细胞器在细胞生物合成和代谢中起主要作用。设计：使用化学固定，高压冷冻和电子显微镜，我们以高倍率对机械压缩的软骨外植体中的软骨细胞进行成像，并定量和定性地评估了分级加载水平导致的细胞器体积和形状的变化。结果：组织受压导致细胞外基质（ECM），软骨细胞，细胞核，粗面内质网和线粒体体积的减少。然而，有趣的是，高尔基体能够抵抗细胞器内水的流失并相对于细胞的其余部分保留其体积的一部分。这些综合结果表明，随着组织受压，细胞内机械梯度和渗透梯度之间的平衡决定了细胞器的形状和体积的变化。结论：我们的结果导致了一个解释性假设，即细胞器体积变化似乎主要是由渗透相互作用驱动的，而形状变化则由结构因素（例如可能与细胞外基质变形相关的细胞骨架相互作用）介导。观察到的软骨细胞器的体积和形状变化以及组织压缩期间细胞器之间的差异行为为连接翻译和翻译后事件（例如高尔基体中糖胺聚糖（GAG）的延伸和硫酸化）的重要机械传递途径提供了证据形变。

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