miR-106a 通过靶向 ATG7 抑制心肌梗死后的自噬和血管生成。
MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction.
机构信息
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.
出版信息
Animal Model Exp Med. 2024 Aug;7(4):408-418. doi: 10.1002/ame2.12418. Epub 2024 May 28.
BACKGROUND
Myocardial infarction (MI) is an acute condition in which the heart muscle dies due to the lack of blood supply. Previous research has suggested that autophagy 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 downstream target gene of miR-106a. The expression of miR-106a and ATG7 was investigated 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.
背景
心肌梗死（MI）是一种由于供血不足导致心肌死亡的急性疾病。先前的研究表明，自噬和血管生成在心肌梗死后预防心力衰竭中起着至关重要的作用，miR-106a 被认为是 MI 中的一个重要调节因子。但具体机制尚不清楚。在这项研究中，我们使用培养的静脉内皮细胞和 MI 大鼠模型，旨在确定 miR-106a 的潜在靶基因，并发现抑制自噬和血管生成的机制。
方法
我们首先探讨了 miR-106a 对内皮细胞自噬和血管生成的生物学功能。然后，我们确定了 ATG7 是 miR-106a 的下游靶基因。在 MI 大鼠模型中研究了 miR-106a 和 ATG7 的表达。
结果
我们发现 miR-106a 抑制静脉内皮细胞的增殖、细胞周期、自噬和血管生成，但促进其凋亡。此外，ATG7 被鉴定为 miR-106a 的靶基因，ATG7 挽救了 miR-106a 对自噬和血管生成的抑制作用。MI 大鼠模型中 miR-106a 的表达降低，但梗死区 ATG7 的表达增加。
结论
我们的结果表明，miR-106a 可能通过靶向 ATG7 来抑制自噬和血管生成。该机制可能是 MI 的一种潜在治疗方法。
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