机构：[1]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China重点科室诊疗科室神经外科神经外科首都医科大学附属天坛医院[2]Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, China神经外科普外科苏州大学附属第二医院[3]China National Clinical Research Center for Neurological Diseases, Beijing, China[4]Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China[5]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China[6]Department of Ophthalmology, School of Medicine, Shandong University, Jinan, China
BACKGROUND: Intracranial aneurysm (IA) is a cerebrovascular disorder characterized by an abnormally bulged artery in the brain and subarachnoid hemorrhage caused by IA rupture with a high ratio of fatality and morbidity. However, the genetic cause of IA remains largely unknown. METHODS: A dysregulated long noncoding RNA (lncRNA) -associated competing endogenous RNA (ceRNA) network was constructed by using sample-matched microRNA (miRNA), lncRNA, and messenger (mRNA) expression profiles in 12 saccular IA samples and paired control arteries. RESULTS: In this study, 1150 lncRNAs, 2545 mRNAs, and 286 miRNAs were differentially expressed in IAs compared with control arteries. Using miRanda, a ceRNA score was assigned, and gene expression methods were used to construct a ceRNA network. The network consists of 8401 miRNA-lncRNA-mRNA interactions (199 miRNAs, 445 lncRNAs, 1116 mRNAs; P < 0.05). Further Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis indicated that the mRNAs involved in the ceRNA network were involved in the regulation of muscle contraction and vascular smooth muscle contraction. CONCLUSIONS: By comparing IAs and their control arteries, we identified differentially expressed lncRNAs, miRNAs, and mRNAs and suggested ceRNA roles in the pathogenesis of IA. These findings may help to characterize the pathogenesis of IA and provide novel therapeutic targets in the future for patients with IA.
基金：
This
research was supported by the following funds: Cooperative
project between The Science and Technology Ministry of China
and Canada titled “Research on the genetics and pathogenesis
of intracranial aneurysm and arteriovenous malformation”, led
by Professor Jizong Zhao (No. 2010 dfb30850); Beijing Municipal
Administration of Hospitals’ Mission Plan (SML20150501); “11th
Five-Year Plan” the National Science and Technology supporting
plan (2006BAI01A13); “13th Five-Year Plan” National Science
and Technology supporting plan (2015BAI09B04); the National
Key Technology Research and Development Program of the
Ministry of Science and Technology of China (2013BAI09B03);
“973” the Ministry of Science and Technology of China
(2012CB825505).
第一作者机构：[1]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China[3]China National Clinical Research Center for Neurological Diseases, Beijing, China[4]Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China[5]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China
共同第一作者：
通讯作者：
通讯机构：[1]Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China[3]China National Clinical Research Center for Neurological Diseases, Beijing, China[4]Center of Stroke, Beijing Institute for Brain Disorders, Beijing, China[5]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China
推荐引用方式(GB/T 7714)：
Hao Li,Wen Wang,Lu Zhang,et al.Identification of a Long Noncoding RNA-Associated Competing Endogenous RNA Network in Intracranial Aneurysm[J].WORLD NEUROSURGERY.2017,97:684-+.doi:10.1016/j.wneu.2016.10.016.
APA：
Hao Li,Wen Wang,Lu Zhang,Qing Lan,Jiangfei Wang...&Jizong Zhao.(2017).Identification of a Long Noncoding RNA-Associated Competing Endogenous RNA Network in Intracranial Aneurysm.WORLD NEUROSURGERY,97,
MLA：
Hao Li,et al."Identification of a Long Noncoding RNA-Associated Competing Endogenous RNA Network in Intracranial Aneurysm".WORLD NEUROSURGERY 97.(2017):684-+
