Department of Cardiology, Liaocheng People's Hospital, Liaocheng, China.
Eur Rev Med Pharmacol Sci. 2018 Sep;22(17):5647-5651. doi: 10.26355/eurrev_201809_15831.
We investigate the effect of long non-coding RNA H19 in acute myocardial infarction (AMI) and the underlying mechanism.
C57BL/6 mice were subjected to AMI and injected with lentivirus pcDNA-H19. After AMI procedures for 3 weeks, cardiac function was detected by echocardiography. The infarct size was stained by triphenyltetrazolium chloride. H19 expression in mice was measured by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Protein expressions of LC3, Beclin-1, and ATG-7 in mice were measured by Western blot.
Our results indicated that H19 expression was significantly downregulated in the infarcted myocardium. Overexpression of H19 after injection with pcDNA-H19 in mice could reduce infarct size and improve cardiac function through upregulating the ratio of LC3-II/I and expressions of Beclin-1 and ATG-7.
Overexpression of H19 could protect AMI in mice via activating autophagy.
研究长链非编码 RNA H19 在急性心肌梗死（AMI）中的作用及其机制。
采用 C57BL/6 小鼠建立 AMI 模型，并注射慢病毒 pcDNA-H19。AMI 术后 3 周，通过超声心动图检测心功能，氯化三苯基四氮唑（TTC）染色检测心肌梗死面积，实时定量聚合酶链反应（qRT-PCR）检测小鼠心肌组织中 H19 的表达，Western blot 检测 LC3、Beclin-1 和 ATG-7 蛋白的表达。
结果表明，H19 在梗死心肌中的表达明显下调。在 pcDNA-H19 注射后，H19 的过表达可以通过上调 LC3-II/I 比值以及 Beclin-1 和 ATG-7 的表达，减少梗死面积，改善心功能。
H19 的过表达可通过激活自噬来保护 AMI 小鼠。
