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首页> 外文期刊>Journal of cellular physiology. >Long noncoding RNA NEAT1 sponges miR-495-3p to enhance myocardial ischemia-reperfusion injury via MAPK6 activation
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Long noncoding RNA NEAT1 sponges miR-495-3p to enhance myocardial ischemia-reperfusion injury via MAPK6 activation

机译：长非编码RNA NEAT1海绵mir - 495 - 3 - p增强心肌缺血再灌注损伤通过MAPK6激活

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摘要

The biological function of long noncoding RNA NEAT1 has been revealed in a lot of diseases. Nevertheless, it is still not yet clear whether NEAT1 can modulate the process of myocardial ischemia-reperfusion injury (M-l/R). Here, we reported that NEAT1 was able to sponge miR-495-3p to contribute to M-l/R injury through activating mitogen-activated protein kinase 6 (MAPK6). First, elevated expression of NEAT1 was revealed in M-l/R injury mice, meanwhile, lactate dehydrogenase (LDH) and creatine kinase-muscle/brain (CK-MB) were also upregulated in the serum. Meanwhile, as previously reported, miR-495 serves as a tumor suppressor or an oncogenic miRNA in different types of cancer. Currently, we found miR-495-3p was remarkably reduced in M-l/R mice. Additionally, NEAT1 was significantly induced whereas miR-495-3p was greatly reduced by H_2O_2 treatment in H9C2 cells. Moreover, loss of NEAT1 in H9C2 cells could repress the viability and proliferation of cells. For another, overexpression of NEAT1 exhibited an opposite phenomenon. Furthermore, LDH release and caspase-3 activity were obviously triggered by upregulation of NEAT1 while suppressed by NEAT1 knockdown. miR-495-3p was indicated and validated as a target of NEAT1 using the analysis of bioinformatics. Interestingly, we observed that miR-495-3p mimics repressed tumor necrosis factor-α (TNF-α), interleukin-lβ (IL-1β ), and IL-18 protein expression while their levels were enhanced by the inhibition of miR-495-3p in H9c2 cells. Subsequently, it was manifested that MAPK6 was a target of miR-495-3p, which could exert a lot in the NEATl/miR-495-3p-mediated M-l/R injury. Overall, our results implied that NEAT1 contributed to M-l/R injury via the modulation of miR-495-3p and MAPK6.
机译：长非编码RNA的生物功能NEAT1被发现在很多疾病。尽管如此,它仍不清楚NEAT1可以调节心肌的过程缺血再灌注损伤(马丁/ R)。报道称,NEAT1能够海绵mir - 495 - 3 - p通过激活为马丁/ R损伤增殖蛋白激酶6 (MAPK6)。首先,NEAT1表达升高了与此同时,在马丁/ R损伤小鼠的乳酸脱氢酶(LDH)和肌酸kinase-muscle /大脑(水平)也被调节在血清中。mir - 495作为一个肿瘤抑制或致癌microrna在不同类型的癌症。目前,我们发现mir - 495 - 3 - p是显著的减少在马丁/ R老鼠。显著诱导而mir - 495 - 3 - p大大减少了H_2O_2在H9C2接受治疗细胞。可以抑制的可行性和扩散细胞。表现出一种相反的现象。LDH释放和caspase-3活动明显由upregulation NEAT1而引发的抑制NEAT1击倒。显示和验证NEAT1作为目标利用生物信息学分析。有趣的是,我们发现mir - 495 - 3 - p模仿抑制肿瘤坏死因子-α(TNF -α),interleukin-lβ(ilβ),和IL-18蛋白表达水平提高了抑制H9c2 mir - 495 - 3 - p的细胞。随后,体现MAPK6是mir - 495 - 3 - p的目标,这可能会产生很多NEATl / mir - 495 - 3 - p -马丁/ R损伤介导的。总的来说,我们的研究结果暗示NEAT1导致了马丁/ R损伤通过调制mir - 495 - 3 - p和MAPK6。

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