DOI: 10.1002/ame2.12418
MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction
Guofeng Bai1
Jinghao Yang2
Weili Liao2
Xiaofeng Zhou3
Yingting He3
Nian Li3
Liuhong Zhang2
Yifei Wang3
Xiaoli Dong4
Hao Zhang3
Jinchun Pan5
Liangxue Lai6
Xiaolong Yuan7
Xilong Wang5
1.Guangdong Provincial Key Laboratory of Laboratory Animals,Guangdong Laboratory Animals Monitoring Institute,Guangzhou,China;Guangdong Laboratory of Lingnan Modern Agriculture,National Engineering Research Center for Breeding Swine Industry,State Key Laboratory of Swine and Poultry Breeding Industry,Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding,College of Animal Science,South China Agricultural University,Guangzhou,Guangdong,China;Huidong County Animal Quarantine and Inspection Institute,Huizhou,Guangdong,China2.Guangdong Provincial Key Laboratory of Laboratory Animals,Guangdong Laboratory Animals Monitoring Institute,Guangzhou,China;Guangdong Laboratory of Lingnan Modern Agriculture,National Engineering Research Center for Breeding Swine Industry,State Key Laboratory of Swine and Poultry Breeding Industry,Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding,College of Animal Science,South China Agricultural University,Guangzhou,Guangdong,China3.Guangdong Laboratory of Lingnan Modern Agriculture,National Engineering Research Center for Breeding Swine Industry,State Key Laboratory of Swine and Poultry Breeding Industry,Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding,College of Animal Science,South China Agricultural University,Guangzhou,Guangdong,China4.Department of Cardiology,Hainan General Hospital,Hainan Affiliated Hospital of Hainan Medical University,Hainan Clinical Medicine Research Institution,Haikou,People's Republic of China5.Guangdong Provincial Key Laboratory of Laboratory Animals,Guangdong Laboratory Animals Monitoring Institute,Guangzhou,China6.Key Laboratory of Regenerative Biology,Guangzhou Institutes of Biomedicine and Health,Chinese Academy of Sciences,Guangzhou,Guangdong,China7.Guangdong Provincial Key Laboratory of Laboratory Animals,Guangdong Laboratory Animals Monitoring Institute,Guangzhou,China;Guangdong Laboratory of Lingnan Modern Agriculture,National Engineering Research Center for Breeding Swine Industry,State Key Laboratory of Swine and Poultry Breeding Industry,Guangdong Provincial Key Laboratory of Agro-Animal Genomics and Molecular Breeding,College of Animal Science,South China Agricultural University,Guangzhou,Guangdong,China;Key Laboratory of Regenerative Biology,Guangzhou Institutes of Biomedicine and Health,Chinese Academy of Sciences,Guangzhou,Guangdong,China
摘要：Background:Myocardial infarction (MI) is an acute condition in which the heart mus-cle dies due to the lack of blood supply.Previous research has suggested that au-tophagy and angiogenesis play vital roles in the prevention of heart failure after MI,and miR-106a is considered to be an important regulatory factor in MI.But the specific mechanism remains unknown.In this study,using cultured venous endothelial cells and a rat model of MI,we aimed to identify the potential target genes of miR-106a and discover the mechanisms of inhibiting autophagy and angiogenesis.
Methods:We first explored the biological functions of miR-106a on autophagy and angiogenesis on endothelial cells.Then we identified ATG7,which was the down-stream target gene of miR-106a .The expression of miR-106a and ATG7 was investi-gated in the rat model of MI.
Results:We found that miR-106a inhibits the proliferation,cell cycle,autophagy and angiogenesis,but promoted the apoptosis of vein endothelial cells.Moreover,ATG7 was identified as the target of miR-106a,and ATG7 rescued the inhibition of autophagy and angiogenesis by miR-106a .The expression of miR-106a in the rat model of MI was decreased but the expression of ATG7 was increased in the infarction areas.
Conclusion:Our results indicate that miR-106a may inhibit autophagy and angiogenesis by targeting ATG7 .This mechanism may be a potential therapeutic treatment for MI.
机标关键词：afterangiogenesisautophagyinfarctioninhibitmyocardialtargets
论文发表日期：2024-08-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：11( 408-418 )
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