Characterization of immortalized human chondrocytes originated from osteoarthritis cartilage.
Characterization of immortalized human chondrocytes originated from osteoarthritis cartilage.
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源自骨关节炎软骨的永生化人类软骨细胞的表征。
DOI：
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发表时间：
2001
影响因子：
5.4
通讯作者：
S. Aizawa
中科院分区：
文献类型：
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作者：
T. Yoshimatsu;A. Saitoh;J. Ryu;D. Shima;H. Handa;M. Hiramoto;Y. Kawakami;S. Aizawa
通过引入含有SV40早期基因的重组SV40-腺病毒载体，从正常人（ch - 4,8， N）和骨关节炎患者（Ch-8-OA）中分离获得了永活克隆的人软骨细胞。这些细胞在单层培养中表现出持续的增殖能力，并表现出软骨细胞的特征，因为它们对碱性磷酸酶和II型胶原呈阳性。当细胞被il -1 α处理时，细胞的生长受到抑制。il -1 α诱导永生化软骨细胞产生IL-6、GM-CSF和TNFalpha。即使在没有il -1 α刺激的情况下，Ch-8-OA细胞也能产生大量的细胞因子，包括IL-6、GM-CSF和TNFalpha。有趣的是，外源添加TNFalpha抑制Ch-8-OA细胞的生长。骨关节炎软骨细胞对各种细胞因子的生物学反应以及这些细胞因子的产生与正常软骨细胞的不同机制，需要进一步的研究来阐明。然而，本研究中建立的新型软骨细胞系可能为研究骨关节炎的发病机制提供一个有用的模型。
Immortalized cloned human chondrocytes isolated from a normal (Ch-4, 8, N) and an osteoarthritis patient (Ch-8-OA) were established by introduction of recombinant SV40-adenovirus vector containing SV40 early gene. These cells exhibited continuous proliferative capacity in monolayer culture and showed chondrocytic characteristics in that they were positive for alkaline phosphatase and collagen type II. When cells were treated with IL-1alpha, the growth was inhibited. IL-1alpha induced the production of IL-6, GM-CSF and TNFalpha from immortalized chondrocytes. Significantly high amounts of cytokines including IL-6, GM-CSF and TNFalpha were produced from Ch-8-OA cells, even in the absence of IL-1alpha stimulation. Interestingly, TNFalpha, exogenously added into the culture, inhibited the growth of Ch-8-OA cells. Further studies are required to clarify the different mechanisms on chondrocytes originating from osteoarthritis cartilage underlying the biological reaction to various cytokines and the production of these cytokines as compared with chondrocytes from normal cartilages. However, the novel chondrocyte cell lines established in the present study may provide researchers with a useful model for studying the pathogenesis of osteoarthritis.