靶向基因的LncRNA260特异性小干扰RNA抑制心肌细胞缺氧/复氧损伤。
LncRNA260-specific siRNA targeting gene inhibit cardiomyocytes hypoxic/reoxygenation injury.
作者信息
Gong Ge, Yang Xin-Xing, Li Yanyan, Geng Hong-Yu, Yang Zhi-Jian, Wang Lian-Sheng, Kim Hyun Jun, Lu Xin-Zheng
机构信息
Department of Gerontology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
出版信息
J Thorac Dis. 2017 Aug;9(8):2447-2460. doi: 10.21037/jtd.2017.07.07.
BACKGROUND
The () gene was indicated to be associated with apoptosis. However, it was not clear whether long non-coding RNA 260 (lncRNA 260)-specific siRNA targeting gene could inhibit hypoxic reoxygenation (H/R) cardiomyocytes injury or not. To explore the mechanisms underlying the protective effects of lncRNA260-specific siRNA-mediated inhibition of IL28RA from H/R injury in cardiomyocytes, the current research was performed.
METHODS
The primary neonatal rat cardiomyocytes were transfected with three different pairs of siRNA specific to lncRNA260 targeting gene and then were undergone with the conditions simulating H/R injury.
RESULTS
All three groups of cardiomyocytes treated with lncRNA260-specific siRNA experienced significantly decreased levels of lactate dehydrogenase activity and apoptosis rate relative to the non-treatment and negative control groups (P<0.05), also expressed reduced levels of IL28RA, and increased levels of PI3KCG and Bcl-2/Bax (P<0.05).
CONCLUSIONS
The lncRNA260-specific siRNA may reduce cardiomyocyte apoptosis associated with H/R injury by decreasing levels of the gene product and thus activating the PI3K/AKT signaling pathway.
背景
（）基因被认为与细胞凋亡有关。然而，靶向该基因的长链非编码RNA 260（lncRNA 260）特异性小干扰RNA（siRNA）是否能抑制缺氧复氧（H/R）诱导的心肌细胞损伤尚不清楚。为了探究lncRNA260特异性siRNA介导的对IL28RA的抑制作用从而保护心肌细胞免受H/R损伤的潜在机制，开展了本研究。
方法
用三对不同的靶向该基因的lncRNA260特异性siRNA转染原代新生大鼠心肌细胞，然后模拟H/R损伤条件进行处理。
结果
相对于未处理组和阴性对照组，所有三组用lncRNA260特异性siRNA处理的心肌细胞的乳酸脱氢酶活性水平和凋亡率均显著降低（P<0.05），IL28RA表达水平降低，PI3KCG和Bcl-2/Bax水平升高（P<0.05）。
结论
lncRNA260特异性siRNA可能通过降低该基因产物水平从而激活PI3K/AKT信号通路来减少与H/R损伤相关的心肌细胞凋亡。
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