The effects of high glucose on tendon-derived stem cells: implications of the pathogenesis of diabetic tendon disorders.
The effects of high glucose on tendon-derived stem cells: implications of the pathogenesis of diabetic tendon disorders.
复制标题
高葡萄糖对肌腱干细胞的影响：糖尿病肌腱疾病发病机制的影响。
DOI：
10.18632/oncotarget.15418
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发表时间：
2017-03-14
期刊：
影响因子：
--
通讯作者：
Teng GJ
中科院分区：
文献类型：
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作者：
Lin YC;Li YJ;Rui YF;Dai GC;Shi L;Xu HL;Ni M;Zhao S;Chen H;Wang C;Li G;Teng GJ
糖尿病患者有很大的风险遭受许多肌肉骨骼疾病，如肌腱病变，肌腱断裂和受损的肌腱愈合。然而，这些肌腱疾病的发病机制仍然不清楚。本研究旨在探讨高糖对体外培养的肌腱源性干细胞（tendon-derived stem cells，TDSCs）增殖、凋亡及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制提供新的见解。采用MTT法和Annexin V-FITC/PI双染法检测各组TDSCs的增殖能力和凋亡率。通过qRT-PCR评估肌腱相关标志物（巩膜轴和胶原I α 1链）的mRNA表达。用蛋白质印迹法检测肌腱相关标志物（Tenomodulin和Collagen I）的蛋白表达。高糖（15 mM和25 mM）处理的TDSCs增殖能力在第1、3和5天明显下降。高糖培养48 h后，TDSCs凋亡率明显增加。高糖处理24 h和48 h后，TDSC中的Scleraxis和Collagen I α 1链基因表达明显降低。高糖处理24 h和48 h后，TDSC中Tenomodulin和CollagenI蛋白表达明显下降。高糖可抑制体外培养的TDSC细胞增殖，诱导细胞凋亡，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病变的病理机制。
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.