Alteration in Long Non-Coding RNA Expression after Traumatic Brain Injury in Rats
Alteration in Long Non-Coding RNA Expression after Traumatic Brain Injury in Rats
复制标题
大鼠脑外伤后长非编码 RNA 表达的变化
DOI：
10.1089/neu.2016.4642
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发表时间：
2017-07-01
影响因子：
4.2
通讯作者：
Jiang, Ji-yao
中科院分区：
文献类型：
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作者：
Wang, Chuan-fang;Zhao, Cheng-cheng;Jiang, Ji-yao
创伤性脑损伤（TBI）引起原发性损伤并引发继发性损伤级联反应。继发性损伤的机制是多因素的，可能包括TBI后长链非编码RNA（lncRNA）的异常表达。在此，进行lncRNA微阵列分析以描绘TBI后大鼠海马中改变的lncRNA。TBI后共有271个lncRNA探针组和1046个信使RNA（mRNA）探针组差异表达。基因本体分析表明，最显着变化的类别的主要成分是炎症，DNA转录，凋亡和坏死性凋亡。此外，通路分析和通路关系网络揭示了主要涉及炎症、细胞周期和凋亡的相关通路。进一步构建了这些异常表达的lncRNA和mRNA的共表达网络，以预测单个lncRNA的潜在功能。前三种lncRNA形成亚共表达网络：NR_002704、ENSRNOT0000062543和Zfas1。因此，我们的研究表明，一系列的lncRNA在大鼠海马TBI后的差异表达，这可能与TBI后的生理和病理过程。这些发现也可能为进一步研究TBI的分子机制和潜在的治疗干预提供新的靶点。
Traumatic brain injury (TBI) causes a primary insult and initiates a secondary injury cascade. The mechanisms underlying the secondary injury are multifactorial and may include the aberrant expression of long non-coding RNA (lncRNA) post-TBI. Here, lncRNA microarray analysis was performed to profile the altered lncRNAs in the rat hippocampus after TBI. A total of 271 lncRNA probe sets and 1046 messenger RNA (mRNA) probe sets were differentially expressed after TBI. Gene ontology analysis showed that the main components of the most significantly changed categories were inflammation, DNA transcription, apoptosis, and necroptosis. Additionally, the pathway analysis and the pathway relation network revealed correlated pathways mainly involving inflammation, cell cycle, and apoptosis. A co-expression network of these aberrantly expressed lncRNAs and mRNAs was further constructed to predict the potential function of individual lncRNAs. Sub-co-expression networks were formed for the top three lncRNAs: NR_002704, ENSRNOT00000062543, and Zfas1. Thus, our study demonstrated differential expression of a series of lncRNAs in the rat hippocampus after TBI, which may be correlated with post-TBI physiological and pathological processes. The findings also may provide novel targets for further investigation of both the molecular mechanisms underlying TBI and potential therapeutic interventions.