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氧化还原调节对培养的大鼠和人肌腱祖细胞增殖、活力及迁移的影响

Effects of Redox Modulation on Cell Proliferation, Viability, and Migration in Cultured Rat and Human Tendon Progenitor Cells.

作者信息

Lee Yuk Wa, Fu Sai Chuen, Yeung Man Yi, Lau Chun Man Lawrence, Chan Kai Ming, Hung Leung Kim

机构信息

Department of Orthopaedics and Traumatology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong.

Department of Orthopaedics and Traumatology, Prince of Wales Hospital, Shatin, Hong Kong.

出版信息

Oxid Med Cell Longev. 2017;2017:8785042. doi: 10.1155/2017/8785042. Epub 2017 Jul 2.

DOI:10.1155/2017/8785042
PMID:28761625
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5518521/
Abstract

Tendon healing is slow and usually results in inferior fibrotic tissue formation. Recently, application of tendon derived stem cells (TDSCs) improved tendon healing in animal studies. In a chicken model, local injection of antioxidants reduced tendon adhesion after tendon injury. An in vitro study demonstrated that supplementation of HO reduced tenogenic marker expression in TDSCs. These findings suggested that the possibility of TDSCs is involved in tendon healing and the cellular activities of TDSCs might be affected by oxidative stress of the local environment. After tendon injury, oxidative stress is increased. Redox modulation might affect healing outcomes via affecting cellular activities in TDSCs. To study the effect of oxidative stress on TDSCs, the cellular activities of rat/human TDSCs were measured under different dosages of vitamin C or HO in this study. Lower dose of vitamin C increased cell proliferation, viability and migration; HO affected colony formation and suppressed cell migration, cell viability, apoptosis, and proliferation. Consistent with previous studies, oxidative stresses (HO) affect both recruitment and survival of TDSCs, while the antioxidant vitamin C may exert beneficial effects at low doses. In conclusion, redox modulation affected cellular activities of TDSCs and might be a potential strategy for tendon healing treatment.

摘要

肌腱愈合缓慢,通常会导致形成劣质的纤维化组织。最近,在动物研究中,应用肌腱衍生干细胞(TDSCs)改善了肌腱愈合。在鸡模型中,局部注射抗氧化剂可减少肌腱损伤后的肌腱粘连。一项体外研究表明,补充HO可降低TDSCs中肌腱生成标志物的表达。这些发现提示,TDSCs参与肌腱愈合,且其细胞活性可能受局部环境氧化应激的影响。肌腱损伤后,氧化应激增加。氧化还原调节可能通过影响TDSCs的细胞活性来影响愈合结果。为研究氧化应激对TDSCs的影响,本研究在不同剂量的维生素C或HO作用下测定了大鼠/人TDSCs的细胞活性。低剂量的维生素C可增加细胞增殖、活力和迁移;HO影响集落形成,并抑制细胞迁移、细胞活力、凋亡和增殖。与先前的研究一致,氧化应激(HO)影响TDSCs的募集和存活,而抗氧化剂维生素C在低剂量时可能发挥有益作用。总之,氧化还原调节影响TDSCs的细胞活性,可能是一种治疗肌腱愈合的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/bf1f76779c2b/OMCL2017-8785042.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/8476b279c5c2/OMCL2017-8785042.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/088837e04808/OMCL2017-8785042.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/bf1f76779c2b/OMCL2017-8785042.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/8476b279c5c2/OMCL2017-8785042.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/088837e04808/OMCL2017-8785042.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee81/5518521/bf1f76779c2b/OMCL2017-8785042.003.jpg

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