RNA‑sequencing analysis of aberrantly expressed long non‑coding RNAs and mRNAs in a mouse model of ventilator‑induced lung injury.
RNA‑sequencing analysis of aberrantly expressed long non‑coding RNAs and mRNAs in a mouse model of ventilator‑induced lung injury.
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呼吸机所致肺损伤小鼠模型中异常表达的长非编码 RNA 和 mRNA 的 RNA 测序分析
DOI：
10.3892/mmr.2018.9034
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发表时间：
2018-07
影响因子：
3.4
通讯作者：
Deng X
中科院分区：
文献类型：
--
作者：
Xu B;Wang Y;Li X;Mao Y;Deng X
长非编码RNAs(Long Non-Coding RNAs，LncRNAs)与多种生物过程的调控密切相关，参与多种疾病的发病。然而，就我们所知，lncRNAs在呼吸机诱导的肺损伤(VILI)中的作用尚未得到评估。在本研究中，高通量测序被应用于研究差异表达的lncRNAs和mRNAs(折叠改变和错误发现率0.05)。生物信息学分析用于预测差异表达的lncRNAs的功能。VILI组肺组织中共有104个lncRNAs(74个上调，30个下调)和809个mRNAs(521个上调，288个下调)差异表达。基因本体论分析表明，差异表达的lncRNAs和mRNAs主要与细胞凋亡、血管生成、中性粒细胞趋化和骨骼肌细胞分化等生物学功能相关。排名前四位的是肿瘤坏死因子信号通路、P53信号通路、神经活性配体-受体相互作用通路和叉头盒O信号通路。据预测，几个lncRNA在VILI中起着至关重要的作用。随后，采用逆转录定量聚合酶链式反应方法，分别检测了3个lncRNAs[丝裂原活化蛋白激酶3，对侧链(Map2k3os)，动力蛋白3，对侧链和含有11个对侧链的脱氢酶结构域]和3个mRNAs(生长停滞和损伤诱导的α、Claudin 4和血栓素A2受体)，以验证测序分析的准确性。此外，map2k3os小干扰核糖核酸可抑制牵张诱导的细胞因子[肿瘤坏死因子α、白介素1β和白介素6]的表达。综上所述，本研究结果提供了VILI中差异表达的lncRNAs图谱。几个重要的lncRNAs可能参与了VILI的病理过程，这可能有助于进一步研究VILI的发病机制。
Long non-coding RNAs (lncRNAs) are closely associated with the regulation of various biological processes and are involved in the pathogenesis of numerous diseases. However, to the best of our knowledge, the role of lncRNAs in ventilator-induced lung injury (VILI) has yet to be evaluated. In the present study, high-throughput sequencing was applied to investigate differentially expressed lncRNAs and mRNAs (fold change >2; false discovery rate <0.05). Bioinformatics analysis was employed to predict the functions of differentially expressed lncRNAs. A total of 104 lncRNAs (74 upregulated and 30 downregulated) and 809 mRNAs (521 upregulated and 288 downregulated) were differentially expressed in lung tissues from the VILI group. Gene ontology analysis demonstrated that the differentially expressed lncRNAs and mRNAs were mainly associated with biological functions, including apoptosis, angiogenesis, neutrophil chemotaxis and skeletal muscle cell differentiation. The top four enriched pathways were the tumor necrosis factor (TNF) signaling pathway, P53 signaling pathway, neuroactive ligand-receptor interaction and the forkhead box O signaling pathway. Several lncRNAs were predicted to serve a vital role in VILI. Subsequently, three lncRNAs [mitogen-activated protein kinase kinase 3, opposite strand (Map2k3os), dynamin 3, opposite strand and abhydrolase domain containing 11, opposite strand] and three mRNAs (growth arrest and DNA damage-inducible α, claudin 4 and thromboxane A2 receptor) were measured by reverse transcription-quantitative polymerase chain reaction, in order to confirm the veracity of RNA-sequencing analysis. In addition, Map2k3os small interfering RNA transfection inhibited the expression of stretch-induced cytokines [TNF-α, interleukin (IL)-1β and IL-6] in MLE12 cells. In conclusion, the results of the present study provided a profile of differentially expressed lncRNAs in VILI. Several important lncRNAs may be involved in the pathological process of VILI, which may be useful to guide further investigation into the pathogenesis for this disease.
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DOI：
10.1016/j.bbrc.2014.03.063
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