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首页> 外文期刊>Journal of Cellular Physiology >Population doublings and percentage of S100-positive cells as predictors of in vitro chondrogenicity of expanded human articular chondrocytes.
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Population doublings and percentage of S100-positive cells as predictors of in vitro chondrogenicity of expanded human articular chondrocytes.

机译：人口倍增和百分比S100-positive细胞作为体外的预测因子chondrogenicity扩大人类的关节软骨细胞。

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The aim of this study was to investigate the interconnection between the processes of proliferation, dedifferentiation, and intrinsic redifferentiation (chondrogenic) capacities of human articular chondrocyte (HAC), and to identify markers linking HAC dedifferentiation status with their chondrogenic potential. Cumulative population doublings (PD) of HAC expanded in monolayer culture were determined, and a threshold range of 3.57-4.19 PD was identified as indicative of HAC loss of intrinsic chondrogenic capacity in pellets incubated without added chondrogenic factors. While several specific gene and surface markers defined early HAC dedifferentiation process, no clear correlation with the loss of intrinsic chondrogenic potential could be established. CD90 expression during HAC monolayer culture revealed two subpopulations, with sorted CD90-negative cells showing lower proliferative capacity and higher chondrogenic potential compared to CD90-positive cells. Although these data further validated PD as critical for in vitro chondrogenesis, due to the early shift in expression, CD90 could not be considered for predicting chondrogenic potential of HAC expanded for several weeks. In contrast, an excellent mathematically modeled correlation was established between PD and the decline of HAC expressing the intracellular marker S100, providing a direct link between the number of cell divisions and dedifferentiation/loss of intrinsic chondrogenic capacity. Based on the dynamics of S100-positive HAC during expansion, we propose asymmetric cell division as a potential mechanism of HAC dedifferentiation, and S100 as a marker to assess chondrogenicity of HAC during expansion, of potential value for cell-based cartilage repair treatments.
机译：本研究的目的是调查过程之间的互连扩散、去分化和内在再分化(chondrogenic)的能力人工关节软骨细胞(HAC),确定去分化标记连接工厂地位与他们chondrogenic潜力。累积人口HAC番(PD)扩大在单层培养测定,和一个阈值范围3.57 - -4.19 PD确认为表明肝固有的损失chondrogenic丸孵化能力没有添加chondrogenic因素。早期和表面标记定义的特定基因HAC去分化过程中,没有明确相关性和内在的损失chondrogenic潜在可能成立。表达HAC在单层培养两个亚种群,CD90-negative排序细胞增殖能力和显示低高chondrogenic潜在相比CD90-positive细胞。验证PD作为体外至关重要软骨形成,由于早期的转变表情,CD90不能考虑预测chondrogenic HAC扩展的潜力几个星期。数学建模相关之间建立PD和HAC的衰落表达的细胞内S100标志,提供的数量之间的直接联系细胞分裂和去分化/损失内在chondrogenic能力。动态S100-positive HAC在扩张,我们建议不对称细胞分裂的HAC的潜在机制去分化S100 HAC的评估chondrogenicity标志在扩张期间,潜在的价值软骨细胞修复疗法。

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