Department of Public Health, Section of Orthopaedics and Trauma Surgery, School of Medicine and Surgery, Federico II University of Naples, Naples, Italy.
Department of Molecular Biology and Medical Biotechnology, School of Medicine and Surgery, Federico II University of Naples, Naples, Italy.
J Biol Regul Homeost Agents. 2016 Oct-Dec;30(4 Suppl 1):115-122.
The aim of our study is to investigate the behaviour of healthy and tendinopathic human tenocytes after a heat shock. After we harvested tendinopathic and healthy human tendon samples, we split tenocytes into 4 groups: 3 groups were submitted to heat shock, followed by different periods of post-heating (2, 4 and 20 h). The other group represents our negative control. The target genes were analysed using Real Time PCR. IL-1β and IL-6 expression were significantly increased in tendinopathic samples after heat shock. COL1 and COL3 expression were increased in non-stimulated tendinopathic tenocytes, but their levels significantly decreased after heat shock (p less than 0.01). COL3 levels increase in healthy samples after 20 h post-heating (p less than 0.01). COL1 and COL3 decreased after heat shock as a sign of the failure of repair mechanisms in tendinopathic tendons. Heat shock in in vitro models was insufficient to trigger pro-inflammatory cytokines in healthy human tenocytes.
我们研究的目的是研究健康和病变人类肌腱细胞在热休克后的行为。在采集病变和健康的人类肌腱样本后,我们将肌腱细胞分为 4 组:3 组接受热休克,然后进行不同时间的加热后处理(2、4 和 20 小时)。另一组是我们的阴性对照。使用实时 PCR 分析靶基因。热休克后,病变样本中的 IL-1β 和 IL-6 表达显著增加。非刺激病变肌腱细胞中的 COL1 和 COL3 表达增加,但热休克后其水平显著降低(p 小于 0.01)。热休克后 20 小时,健康样本中的 COL3 水平增加(p 小于 0.01)。COL1 和 COL3 在热休克后减少,表明病变肌腱的修复机制失败。体外模型中的热休克不足以在健康的人类肌腱细胞中引发促炎细胞因子。