期刊论文详细信息
BMC Immunology
Mesenchymal stem cell conditioned medium alleviates oxidative stress injury induced by hydrogen peroxide via regulating miR143 and its target protein in hepatocytes
Research Article
Dong Li1  Xue Li1  Qing Shi1  Xuejing Xu2  Xiuli Ju2 
[1] Department of Pediatrics, Qilu Hospital, Shandong University, 250012, Jinan, China;Shenzhen Research Institute of Shandong University, 518057, Shenzhen, China;Department of Pediatrics, Qilu Hospital, Shandong University, 250012, Jinan, China;
关键词: Hepatocyte;    Oxidative stress injury;    Mesenchymal stem cell;    miRNA;    Apoptosis;   
DOI  :  10.1186/s12865-017-0232-x
 received in 2017-02-18, accepted in 2017-12-06,  发布年份 2017
来源: Springer
PDF
【 摘 要 】

BackgroundTo investigate the impact of miRNA (microRNA) on hepatic oxidative stress damage under the human mesenchymal stem cell conditioned medium (MSC-CM) and explore the roles of the beta-1 adrenergic receptor (ADRB1) and hexokinase 2 (HK2) in this process.MethodsHydrogen peroxide was used to induce oxidative stress injury in the human normal liver cell line L02. MSC-CM was separately prepared. After treatment with MSC-CM, the protective effects of MSC-CM on oxidative stress injury were assessed by changes in apoptosis, cell viability, cell cycle, and mitochondrial membrane potential. According to the microarray analysis, 19 disparately expressed miRNAs were selected for RT-PCR and miR143 identified as having significant differential expression in MSC-CM against oxidative stress injury. Subsequently, the predicted target proteins of miR143 were selected by bioinformatics software, and verified by western blot. In addition, down-regulation and up-regulation of miR143 expression and hydrogen peroxide induced hypoxia injury were carried out on L02 cells to study the role of miR143.ResultsMSC-CM significantly attenuated H2O2 induced oxidative stress injury. The expression of miR143 was increased following oxidative stress injury whereas it decreased after MSC-CM treatment. The expression levels of HK2 and ADRB1 regulated by miR143 and Bcl-2 decreased under H2O2 treatment but were restored following MSC-CM treatment. However the expression levels of Bax and BMF increased after H2O2 injury and decreased after MSC-CM treatment. Moreover over-expression or down-regulation of miR143 aggravated or alleviated hepatocyte apoptosis respectively.ConclusionsMSC-CM may alleviate H2O2 induced oxidative stress injury by inhibiting apoptosis and adjusting miRNA expression. Moreover down-regulation of miR143 protects L02 cells from apoptosis and initiates an adaptive process by adjusting the expression of HK2 ADRB1 and apoptosis-related proteins.

【 授权许可】

CC BY   
© The Author(s). 2017

【 预 览 】
附件列表
Files Size Format View
RO202311101118347ZK.pdf 3092KB PDF download
【 参考文献 】
  • [1]
  • [2]
  • [3]
  • [4]
  • [5]
  • [6]
  • [7]
  • [8]
  • [9]
  • [10]
  • [11]
  • [12]
  • [13]
  • [14]
  • [15]
  • [16]
  • [17]
  • [18]
  • [19]
  • [20]
  • [21]
  • [22]
  • [23]
  • [24]
  • [25]
  • [26]
  • [27]
  • [28]
  • [29]
  • [30]
  • [31]
  • [32]
  • [33]
  • [34]
  • [35]
  • [36]
  • [37]
  • [38]
  • [39]
  • [40]
  • [41]
  • [42]
  • [43]
  • [44]
  • [45]
  • [46]
  • [47]
  • [48]
  • [49]
  文献评价指标  
  下载次数:5次 浏览次数:0次