...
首页> 外文期刊>Rheumatology international. >Investigation of chondrocyte hypertrophy and cartilage calcification in a full-depth articular cartilage explants model
【24h】

Investigation of chondrocyte hypertrophy and cartilage calcification in a full-depth articular cartilage explants model

机译:全深度关节软骨外植体模型中软骨细胞肥大和软骨钙化的研究

获取原文
获取原文并翻译 | 示例

摘要

Articular cartilage deterioration, which includes cartilage degradation and chondrocyte hypertrophy, is a hallmark of degenerative joint diseases (DJD). Chondrocyte hypertrophy is initiated in the deep layer of the cartilage; thus, a robust explants model for investigation of hypertrophy should include this zone. The aim of this study was to characterize and investigate the hypertrophy-promoting potential of different endogenous factors on an ex vivo articular cartilage model. The full-depth cartilage explants were harvested from bovine femoral condyle and cultured for 13 days in different conditions: 10 ng/ml oncostatin M + 20 ng/ml TNF-??; 100 ng/ml IGF1; 10-100 ng/ml bFGF; 10-100 ng/ml BMP2; 50 ??g/ml ascorbic acid in combination with 10 mM ??-glycerophosphate; and 20-100 ng/ml triiodothyronine. The cellular activity and morphology, degradation, formation and calcification, and expression level of hypertrophic markers were investigated. The hypertrophic factors tested all induced cellular activity and marked morphological changes starting at day 4, however, not in a synchronized manner. Both cartilage degradation and formation were induced by T3 (P < 0.05). Only T3 had a full hypertrophic gene expression profile (P < 0.05). We developed and characterized a novel model for investigation of chondrocyte hypertrophy. We speculated that this can become an important investigatory tool for investigation of matrix turnover, chondrocyte hypertrophy and cartilage calcification that are associated with DJD pathogenesis. ? 2012 Springer-Verlag.
机译:关节软骨退化,包括软骨退化和软骨细胞肥大,是退行性关节疾病(DJD)的标志。软骨细胞肥大在软骨的深层开始。因此,用于研究肥大的健壮外植体模型应包括该区域。这项研究的目的是表征和研究离体关节软骨模型上不同内源性因素促进肥大的潜力。从牛股骨dy中收获全深度的软骨外植体,并在不同条件下培养13天:10 ng / ml抑瘤素M + 20 ng / mlTNF-α。 100 ng / ml IGF1; 10-100 ng / ml bFGF; 10-100 ng / ml BMP2; 50μg/ ml抗坏血酸与10 mMα-甘油磷酸的混合物;和20-100 ng / ml三碘甲状腺素。研究了肥大标志物的细胞活性和形态,降解,形成和钙化以及表达水平。肥厚因子从第4天开始测试所有诱导的细胞活性和显着的形态变化,但并非以同步方式进行。 T3诱导软骨降解和形成(P <0.05)。仅T3具有完整的肥大基因表达谱(P <0.05)。我们开发并表征了一种新型的软骨细胞肥大研究模型。我们推测,这可以成为调查与DJD发病机制相关的基质更新,软骨细胞肥大和软骨钙化的重要研究工具。 ? 2012年,施普林格出版社。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号