首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Long noncoding RNAs interact with mRNAs: A new perspective on the mechanism of premature brain injury
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Long noncoding RNAs interact with mRNAs: A new perspective on the mechanism of premature brain injury

机译:长的非编码RNA与MRNA相互作用:一种新的脑损伤机制的新视角

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The molecular mechanism of premature brain injury induced by inflammation is not fully understood. Long noncoding RNAs (lncRNAs) have been reported to play crucial roles in neurological disorders including brain injury. However, little is known about the regulatory function of lncRNAs in the premature brain. This study investigates differentially expressed lncRNAs and mRNAs as well as their interactions in the premature brain. Lipopolysaccharides (LPS) were used to induce inflammation in premature rodent models. Brain histology was observed via hematoxylin and eosin (HE) staining and CD68 immunostaining. Arraystar microarry was designed for the profiling of differentially expressed lncRNAs and mRNAs in 4 LPS induced premature brains (L group), 4 full-term control brains (C group) and 3 premature brains were not induced by LPS (P group). Bioinformatic analysis was applied to reveal the functions and co-expression relationship of lncRNAs and mRNAs. Three lncRNAs and 2 mRNAs were selected for validation applying quantitative real time polymerase chain reaction (qRT-PCR). This study demonstrates dysregulated lncRNA and mRNA profiles in the premature brains upon inflammatory insult, thus revealing a novel mechanism of premature brain development from a new perspective of the lncRNAs and mRNA coexpression network and providing important insights into the therapy of premature brain injury.
机译:由炎症引起的早产脑损伤的分子机制尚不完全清楚。长非编码RNA(lncRNAs)已报道在神经系统疾病,包括脑损伤中发挥重要作用。然而,鲜为人知的是,lncRNAs的过早大脑的调节功能。这项研究调查了过早的大脑差异表达lncRNAs和mRNA的,以及它们之间的相互作用。脂多糖(LPS)被用于诱导早产啮齿动物模型中的炎症。通过苏木精和伊红(HE)染色和免疫染色CD68观察到脑的组织学。 Arraystar微阵列被设计为差异表达lncRNAs和mRNA的4个LPS仿形诱导早产的大脑(L基团),4足月对照脑中(C组)和3个过早大脑不是由LPS(P组)诱导。施加生物信息学分析以显示功能和lncRNAs和mRNA的共表达的关系。被选择用于施加定量实时聚合酶链式反应(qRT-PCR)验证三个lncRNAs和2倍的mRNA。这项研究表明失调lncRNA和表达谱中在炎症刺激过早的大脑,从而揭示从ln​​cRNAs和mRNA共表达网络的一个新的视角大脑过早发育的新机制,并提供了重要的见解大脑过早损伤的治疗。

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