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首页> 外文期刊>Osteoarthritis and cartilage >Characterization of mature vs aged rabbit articular cartilage: analysis of cell density, apoptosis-related gene expression and mechanisms controlling chondrocyte apoptosis.
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Characterization of mature vs aged rabbit articular cartilage: analysis of cell density, apoptosis-related gene expression and mechanisms controlling chondrocyte apoptosis.

机译：成熟与衰老兔关节软骨的特征：细胞密度，凋亡相关基因表达和控制软骨细胞凋亡机制的分析。

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OBJECTIVE: The prevalence of osteoarthritis (OA) is increased in aged individuals and a direct correlation between chondrocyte apoptosis and cartilage degradation secondary to OA has been demonstrated. To address the question of whether age predisposes articular cartilage to apoptosis, the objective of the present study was to characterize and compare in aged and mature non-OA rabbit articular cartilage, cell density and expression levels of specific genes associated with apoptosis. Mechanistic studies on the inhibition of induced apoptosis were also carried out. METHODS: Grade I (non-OA) femoral condyles and tibial plateaus from mature and aged rabbits were taken for assessment of viable cell density (VCD) and mRNA (reverse transcription-polymerase chain reaction) expression levels of the pro-apoptotic genes, Fas, Fas ligand (FasL), caspase-8, inducible nitric oxide synthase (iNOS) and p53. In vitro insulin-like growth factor (IGF-1)-mediated inhibition of nitric oxide (NO)-induced apoptosis was also examined using sodium nitroprusside (SNP) as NO donor. RESULTS: VCD was decreased 50-70% in aged articular cartilage relative to mature cartilage. mRNA expression levels of Fas, FasL, caspase-8 and p53 were higher in aged cartilage than in mature cartilage. iNOS expression was unchanged. IGF-1-mediated inhibition of NO-induced apoptosis was dose-dependent and reversed with addition of phosphatidylinositol-3 kinase inhibitor. CONCLUSIONS: This controlled animal model study demonstrates that age predisposes articular cartilage to changes in VCD and expression levels of specific pro-apoptotic genes. It is significant that these findings were demonstrated on cartilage that showed no prior signs of OA; it is also possible that such changes are a prelude to the age-related development of OA.
机译：目的：老年人骨关节炎（OA）的患病率增加，并且已证明软骨细胞凋亡与继发于OA的软骨降解之间存在直接相关性。为了解决年龄是否使关节软骨易于发生凋亡的问题，本研究的目的是表征和比较老年和成熟的非OA兔关节软骨，细胞密度以及与凋亡相关的特定基因的表达水平。还进行了抑制诱导的细胞凋亡的机理研究。方法：取成年和成年兔的I级（非OA）股骨con和胫骨平台，评估促凋亡基因Fas的活细胞密度（VCD）和mRNA（逆转录-聚合酶链反应）表达水平。 ，Fas配体（FasL），caspase-8，诱导型一氧化氮合酶（iNOS）和p53。还使用硝普钠（SNP）作为NO供体检查了胰岛素样生长因子（IGF-1）介导的一氧化氮（NO）诱导的细胞凋亡的抑制作用。结果：与成熟软骨相比，老年关节软骨的VCD降低了50-70％。老年软骨中Fas，FasL，caspase-8和p53的mRNA表达水平高于成熟软骨。 iNOS表达未改变。 IGF-1介导的NO诱导的细胞凋亡抑制作用是剂量依赖性的，并通过添加磷脂酰肌醇3激酶抑制剂逆转。结论：这项受控动物模型研究表明年龄易使关节软骨受到VCD变化和特定促凋亡基因表达水平的影响。重要的是，这些发现在没有先兆OA迹象的软骨上得到了证实;这种变化也可能是与年龄有关的OA发展的前奏。

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