抑制长链非编码 RNA TTTY15 通过靶向 miR-455-5p 减轻低氧诱导的心肌细胞损伤。
Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p.
机构信息
Department of Cardiology, Changhai Hospital, Second Military Medical University, No 168 Changhai Road, Shanghai 200433, China.
Department of Cardiology, Changhai Hospital, Second Military Medical University, No 168 Changhai Road, Shanghai 200433, China; Department of Cardiology, Jing'an District Centre Hospital of Shanghai, Fudan University, Shanghai, 200040, China.
出版信息
Gene. 2019 Jun 15;701:1-8. doi: 10.1016/j.gene.2019.02.098. Epub 2019 Mar 18.
Myocardial infarction (MI) is a severe heart disease caused by acute, persistent ischemia or hypoxia and finally leads to heart failure and sudden death. However, the intrinsic molecular mechanisms of MI remain largely unknown. lncRNAs have also been implicated in the process of ischemic heart diseases. However, the role of lncRNA TTTY15 in MI is not elucidated. We evaluated the expression of TTTY15 in MI and human cardiomyocyte under hypoxia. We explored the role of TTTY15 in cell injury under hypoxia. We searched for potential target of TTTY15. Up-regulation of TTTY15 was associated with hypoxia. Silencing TTTY15 prevented hypoxia-induced cell apoptosis and rescued the cell migration and invasion. TTTY15 targeted miR-455-5p, which regulated the Jun dimerization protein 2 (JDP2) expression. Knocking down miR-455-5p abolished effects of TTTY-15 silencing on cell injury. Suppression of long noncoding RNA TTTY15 attenuates hypoxia-induced cardiomyocytes injury by targeting miR-455-5p.
心肌梗死（MI）是一种由急性、持续缺血或缺氧引起的严重心脏病，最终导致心力衰竭和猝死。然而，MI 的内在分子机制在很大程度上尚不清楚。lncRNAs 也被认为与缺血性心脏病的发生有关。然而，lncRNA TTTY15 在 MI 中的作用尚未阐明。我们评估了 TTTY15 在 MI 和缺氧状态下人心肌细胞中的表达。我们探讨了 TTTY15 在缺氧状态下对细胞损伤的作用。我们寻找 TTTY15 的潜在靶标。TTTY15 的上调与缺氧有关。沉默 TTTY15 可防止缺氧诱导的细胞凋亡，并挽救细胞迁移和侵袭。TTTY15 靶向 miR-455-5p，后者调节 Jun 二聚化蛋白 2（JDP2）的表达。敲低 miR-455-5p 可消除 TTTY-15 沉默对细胞损伤的影响。抑制长非编码 RNA TTTY15 通过靶向 miR-455-5p 减轻缺氧诱导的心肌细胞损伤。
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