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鲽源钙素2通过抑制氧化应激增强间充质干细胞的存活能力。

Stanniocalcin 2 enhances mesenchymal stem cell survival by suppressing oxidative stress.

作者信息

Kim Pyung-Hwan, Na Sang-Su, Lee Bomnaerin, Kim Joo-Hyun, Cho Je-Yoel

机构信息

Department of Biomedical Laboratory Science, College of Medical Science, Konyang University, Daejeon 35365, Korea; Department of Biochemistry, BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.

Department of Biochemistry, BK21 PLUS Program for Creative Veterinary Science Research, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.

出版信息

BMB Rep. 2015 Dec;48(12):702-7. doi: 10.5483/bmbrep.2015.48.12.158.

Abstract

To overcome the disadvantages of stem cell-based cell therapy like low cell survival at the disease site, we used stanniocalcin 2 (STC2), a family of secreted glycoprotein hormones that function to inhibit apoptosis and oxidative damage and to induce proliferation. STC2 gene was transfected into two kinds of stem cells to prolong cell survival and protect the cells from the damage by oxidative stress. The stem cells expressing STC2 exhibited increased cell viability and improved cell survival as well as elevated expression of the pluripotency and self-renewal markers (Oct4 and Nanog) under sub-lethal oxidative conditions. Up-regulation of CDK2 and CDK4 and down-regulation of cell cycle inhibitors p16 and p21 were observed after the delivery of STC2. Furthermore, STC2 transduction activated pAKT and pERK 1/2 signal pathways. Taken together, the STC2 can be used to enhance cell survival and maintain long-term stemness in therapeutic use of stem cells.

摘要

为克服基于干细胞的细胞疗法的缺点,如疾病部位细胞存活率低,我们使用了2型鲽鱼钙蛋白(STC2),它是一类分泌型糖蛋白激素,具有抑制细胞凋亡和氧化损伤以及诱导细胞增殖的功能。将STC2基因转染到两种干细胞中,以延长细胞存活时间并保护细胞免受氧化应激的损伤。在亚致死性氧化条件下,表达STC2的干细胞表现出细胞活力增加、细胞存活率提高以及多能性和自我更新标志物(Oct4和Nanog)的表达升高。在导入STC2后,观察到细胞周期蛋白依赖性激酶2(CDK2)和细胞周期蛋白依赖性激酶4(CDK4)上调,细胞周期抑制剂p16和p21下调。此外,STC2转导激活了pAKT和pERK 1/2信号通路。综上所述,STC2可用于提高干细胞治疗应用中的细胞存活率并维持长期干性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6db4/4791327/3d644fe2412b/BMB-48-702-g001.jpg

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