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 | |
【 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 】
Files | Size | Format | View |
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RO202311101118347ZK.pdf | 3092KB | download |
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