MiR-125a靶向GDF11调控缺氧复氧肝细胞损伤修复的机制  

Mechanism of miR-125a regulates the injury and repair of hypoxia-reoxygenation hepatocytes by targeting GDF11

作　　者：张志标[1] 余伟[2] 马达[2] 刘礼军[2] ZHANG Zhibiao;YU Wei;MA Da;LIU Lijun(Department of Emergency,Hanchuan People’s Hospital,Wuhan 431600,China;Second Department of General Surgery,Hanchuan People’s Hospital,Wuhan 431600,China)

机构地区：[1]汉川市人民医院急诊科,武汉431600 [2]汉川市人民医院普外科二科,武汉431600

出　　处：《临床与病理杂志》2019年第2期244-251,共8页Journal of Clinical and Pathological Research

摘　　要：目的:探究miR-125a靶向生长分化因子11(growth differentiation factor 11,GDF11)调控缺氧复氧肝细胞损伤修复的机制。方法:建立肝细胞L02的缺氧复氧模型;RT-q PCR和Western印迹检测miR-125a和GDF11在缺氧复氧肝细胞中的表达;双荧光素报告基因实验验证miR-125a与GDF11的靶向关系;MTT法和流式细胞技术检测上调miR-125a和敲低GDF11表达对缺氧复氧肝细胞的影响;Western印迹检测细胞凋亡因子Bax,Bcl-2,caspase-3在缺氧复氧肝细胞中的表达。结果:在缺氧复氧肝细胞中,miR-125a表达下调,GDF11表达则显著上调;上调miR-125a和敲低GDF11表达可增强缺氧复氧肝细胞的活力,抑制凋亡;GDF11是miR-125a的靶基因,且miR-125a通过负性调控GDF11的表达影响缺氧复氧肝细胞的凋亡,GDF11可逆转miR-125a对缺氧复氧肝细胞凋亡相关分子表达的影响。结论:miR-125a靶向GDF11参与缺氧复氧肝细胞的损伤修复过程。Objective:To explore the mechanism of miR-125a regulates the injury and repair of hypoxia-reoxygenation hepatocytes by targeting growth differentiation factor 11(GDF11).Methods:The hypoxia-reoxygenation model of hepatocyte L02 was established;the expression of miR-125a and GDF11 in hypoxia-reoxygenation hepatocytes was detected by RT-qPCR and Western blot;the targeting relationship between miR-125a and GDF11 was measured by double fluorescein reporter gene assay;the effects of upregulation of miR-125a and knockdown of GDF11 on hypoxia-reoxygenation hepatocytes were estimated by MTT and flow cytometry;Western blot was performed to the expression of apoptosis factors Bax,Bcl-2 and caspase-3 in anoxia reoxygenation hepatocytes.Results:In hypoxic-reoxygenated hepatocytes,the expression of miR-125a was downregulated,while the expression of GDF11 was upregulated significantly;upregulation of miR-125a or knockdown of GDF11 enhanced the viability and inhibited apoptosis of hypoxic-reoxygenated hepatocytes;GDF11 was the target gene of miR-125a,and miR-125a negatively regulated the expression of GDF11 in hypoxic-reoxygenated hepatocytes.GDF11 reversed the effect of miR-125a on expression of apoptosis related molecules in anoxia reoxygenation hepatocytes.Conclusion:MiR-125a participates in the injury and repair of anoxia reoxygenation hepatocytes by targeting GDF11.

关 键 词：miR-125a 生长分化因子11 缺氧复氧 凋亡 肝细胞 

分 类 号：R657.3[医药卫生—外科学]