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高密度软骨细胞培养中软骨对机械力的反应

Cartilage response to mechanical force in high-density chondrocyte cultures.

作者信息

van Kampen G P, Veldhuijzen J P, Kuijer R, van de Stadt R J, Schipper C A

出版信息

Arthritis Rheum. 1985 Apr;28(4):419-24. doi: 10.1002/art.1780280410.

DOI:10.1002/art.1780280410
PMID:3986007
Abstract

High-density cultures of chick embryonic chondrocytes were exposed to intermittent compressive force (ICF) of physiologic magnitude for 24 hours. Proteoglycan synthesis was significantly increased in chondrocyte cultures exposed to ICF as compared with control cultures. Similar effects were found in explants of epiphyseal cartilage. Proteoglycans extracted with guanidine-HCl from cultures exposed to ICF aggregated better with hyaluronic acid than did control cultures, as shown by Sepharose 2B gel chromatography. In addition, the amount of non-extractable proteoglycans was increased in ICF cultures. We conclude that ICF not only increases the synthesis of proteoglycans but also improves the aggregating capacity of proteoglycans and the coherence of proteoglycans with other matrix components. High-density cultures of epiphyseal chondrocytes provide a suitable model to study the processes involved in the perception of and the subsequent cellular response to compressive force by cartilage.

摘要

将鸡胚软骨细胞的高密度培养物暴露于生理强度的间歇性压缩力(ICF)下24小时。与对照培养物相比,暴露于ICF的软骨细胞培养物中蛋白聚糖的合成显著增加。在骨骺软骨外植体中也发现了类似的效果。通过琼脂糖2B凝胶色谱法显示,用盐酸胍从暴露于ICF的培养物中提取的蛋白聚糖与透明质酸的聚集性比对照培养物更好。此外,ICF培养物中不可提取的蛋白聚糖量增加。我们得出结论,ICF不仅增加了蛋白聚糖的合成,还提高了蛋白聚糖的聚集能力以及蛋白聚糖与其他基质成分的黏附性。骨骺软骨细胞的高密度培养提供了一个合适的模型,用于研究软骨对压缩力的感知过程以及随后的细胞反应。

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Cartilage response to mechanical force in high-density chondrocyte cultures.高密度软骨细胞培养中软骨对机械力的反应
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Hydrostatic pressure induces expression of interleukin 6 and tumour necrosis factor alpha mRNAs in a chondrocyte-like cell line.流体静压力可诱导类软骨细胞系中白细胞介素6和肿瘤坏死因子α信使核糖核酸的表达。
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Damage to type II collagen in aging and osteoarthritis starts at the articular surface, originates around chondrocytes, and extends into the cartilage with progressive degeneration.衰老和骨关节炎中II型胶原蛋白的损伤始于关节表面,起源于软骨细胞周围,并随着软骨的逐渐退变延伸至软骨内部。
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