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The effects of high glucose on tendon-derived stem cells: implications of the pathogenesis of diabetic tendon disorders

机译:高糖对肌腱衍生干细胞的影响:糖尿病肌腱疾病发病机理的启示

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摘要

Patients with diabetes are at great risk to suffer many musculoskeletal disorders, such as tendinopathy, tendon rupture and impaired tendon healing. However, the pathogenesis of these tendon disorders still remains unclear. In this study, we aimed to investigate the effects of high glucose on cell proliferation, cell apoptosis and tendon-related markers expression of tendon-derived stem cells (TDSCs) in vitro. These findings might provide new insights into the pathogenesis of diabetic tendon disorders. The cell proliferative ability and apoptosis rate of TDSCs in different groups were evaluated by MTT assay and Annexin V-FITC/PI staining assay. The mRNA expression of tendon-related markers (Scleraxis and Collagen I alpha 1 chain) were assessed by qRT-PCR. The protein expression of tendon-related markers (Tenomodulin and Collagen I) were measured by Western blotting. The proliferative ability of TDSCs treated with high glucose (15mM and 25mM) decreased significantly at day1, day3 and day5. The cell apoptosis of TDSCs increased significantly when they were cultured with high glucose for 48h in vitro. The gene expression of Scleraxis and Collagen I alpha 1 chain in TDSCs decreased significantly when they were treated with high glucose for 24h and 48h. The protein expression of Tenomodulin and Collagen I in TDSCs decreased significantly when they were treated with high glucose for 24h and 48h. High glucose could inhibit cell proliferation, induce cell apoptosis and suppress the tendon-related markers expression of TDSCs in vitro. These findings might account for some pathological mechanisms underlying the pathogenesis of diabetic tendon disorders.
机译:糖尿病患者极易遭受许多肌肉骨骼疾病的困扰,例如肌腱病,肌腱破裂和肌腱愈合受损。但是,这些肌腱疾病的发病机理仍不清楚。在这项研究中,我们旨在研究高糖对肌腱干细胞(TDSCs)体外细胞增殖,细胞凋亡和肌腱相关标志物表达的影响。这些发现可能为糖尿病肌腱疾病的发病机理提供新的见解。用MTT法和膜联蛋白V-FITC / PI染色法评价不同组TDSCs的细胞增殖能力和凋亡率。通过qRT-PCR评估肌腱相关标志物(Scleraxis和胶原Iα1链)的mRNA表达。通过蛋白质印迹法测量肌腱相关标记(Tenomodulin和胶原I)的蛋白表达。高葡萄糖(15mM和25mM)处理的TDSCs的增殖能力在第1天,第3天和第5天显着下降。 TDSCs在体外高糖培养48h后,其细胞凋亡明显增加。用高糖处理24h和48h时,TDSCs中Scleraxis和I型胶原1链的基因表达显着下降。高糖处理24h和48h后,TDSCs中Tenomodulin和胶原I的蛋白表达显着下降。高糖可以抑制TDSCs的体外增殖,诱导细胞凋亡并抑制肌腱相关标志物的表达。这些发现可能解释了糖尿病肌腱疾病发病机理的一些病理机制。

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