Thioredoxin-1 Protects Bone Marrow-Derived Mesenchymal Stromal Cells from Hyperoxia-Induced Injury In Vitro.
Thioredoxin-1 Protects Bone Marrow-Derived Mesenchymal Stromal Cells from Hyperoxia-Induced Injury In Vitro.
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Thioredoxin-1 保护骨髓来源的间充质基质细胞免受高氧诱导的体外损伤
DOI：
10.1155/2018/1023025
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发表时间：
2018
影响因子：
--
通讯作者：
Wang L
中科院分区：
文献类型：
--
作者：
Zhang L;Wang J;Chen Y;Zeng L;Li Q;Liu Y;Wang L
移植到受体肺部的间充质基质细胞（MSC）的存活率很低，极大地限制了它们对支气管肺发育不良（BPD）等疾病的治疗效果。本研究的目的是评估硫氧还蛋白-1 (Trx-1) 过度表达对提高骨髓间充质基质细胞 (BMSC) 抵抗高氧诱导的细胞损伤的潜力的影响。 使用80% O2 模拟体外高氧肺损伤中移植细胞周围的微环境。测量 BMSC 增殖和凋亡率以及活性氧 (ROS) 水平。研究了Trx-1过表达对抗氧化剂和生长因子水平的影响。我们还研究了凋亡调节激酶 1 (ASK1) 和 p38 丝裂原激活蛋白激酶 (MAPK) 的激活。 Trx-1 过表达显着减少高氧诱导的 BMSC 凋亡并增加细胞增殖。我们证明，Trx-1 过表达会上调超氧化物歧化酶和谷胱甘肽过氧化物酶的水平，并下调 ROS 的产生。此外，我们还发现 Trx-1 通过降低 ASK1/P38 MAPK 激活率来保护 BMSC 免受高氧损伤。 这些结果表明，Trx-1 过表达提高了 BMSC 抵抗高氧诱导损伤的能力，从而增加了它们治疗高氧诱导肺部疾病（如 BPD）的潜力。
The poor survival rate of mesenchymal stromal cells (MSC) transplanted into recipient lungs greatly limits their therapeutic efficacy for diseases like bronchopulmonary dysplasia (BPD). The aim of this study is to evaluate the effect of thioredoxin-1 (Trx-1) overexpression on improving the potential for bone marrow-derived mesenchymal stromal cells (BMSCs) to confer resistance against hyperoxia-induced cell injury. 80% O2 was used to imitate the microenvironment surrounding-transplanted cells in the hyperoxia-induced lung injury in vitro. BMSC proliferation and apoptotic rates and the levels of reactive oxygen species (ROS) were measured. The effects of Trx-1 overexpression on the level of antioxidants and growth factors were investigated. We also investigated the activation of apoptosis-regulating kinase-1 (ASK1) and p38 mitogen-activated protein kinases (MAPK). Trx-1 overexpression significantly reduced hyperoxia-induced BMSC apoptosis and increased cell proliferation. We demonstrated that Trx-1 overexpression upregulated the levels of superoxide dismutase and glutathione peroxidase as well as downregulated the production of ROS. Furthermore, we illustrated that Trx-1 protected BMSCs against hyperoxic injury via decreasing the ASK1/P38 MAPK activation rate. These results demonstrate that Trx-1 overexpression improved the ability of BMSCs to counteract hyperoxia-induced injury, thus increasing their potential to treat hyperoxia-induced lung diseases such as BPD.
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DOI：
10.1164/rccm.200902-0242oc
发表时间：
2009-12-01
影响因子：
24.7
作者：
Aslam, Muhammad;Baveja, Rajiv;Kourembanas, Stella
通讯作者：
Kourembanas, Stella
问家族蛋白在压力反应和疾病中的作用。
DOI：
10.1186/1478-811x-7-9
发表时间：
2009-04-24
期刊：
Cell communication and signaling : CCS
影响因子：
--
作者：
Hattori K;Naguro I;Runchel C;Ichijo H
通讯作者：
Ichijo H
硫氧还蛋白保护胎儿 II 型上皮细胞免受高氧诱导的损伤
影响因子：
3.1
作者：
Chen, Yan;Chang, Liwen;Pan, Rui
通讯作者：
Pan, Rui
影响因子：
3.7
作者：
Dai, Xueling;Sun, Yaxuan;Jiang, Zhaofeng
通讯作者：
Jiang, Zhaofeng
影响因子：
37.8
作者：
Barbash, IM;Chouraqui, P;Leor, J
通讯作者：
Leor, J