Analysis of Long Non-Coding RNA Expression of Lymphatic Endothelial Cells in Response to Type 2 Diabetes

被引:39
作者
Qi, Min [1 ]
Zhou, Qiuhong [2 ]
Zeng, Weiqi [3 ]
Shen, Minxue [3 ]
Liu, Xiaomin [2 ]
Luo, Chang [3 ]
Long, Jing [3 ]
Chen, Wangqing [3 ]
Yan, Siyu [3 ]
Zhang, Jianglin [3 ]
机构
[1] Cent S Univ, Xiangya Hosp, Dept Plast Surg, Changsha, Hunan, Peoples R China
[2] Cent S Univ, Xiangya Hosp, Dept Endocrinol, Changsha, Hunan, Peoples R China
[3] Cent S Univ, Xiangya Hosp, Dept Dermatol, 87 Xiangya Rd, Changsha 410008, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
Lymphatic endothelial cells; Type; 2; diabetes; Long non-coding RNA; H19; TRANSCRIPTION FACTORS; DYSFUNCTION; MECHANISMS; PROFILES;
D O I
10.1159/000456599
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background: Recent evidence has indicated that long non-coding RNA (lncRNA) is involved in the pathogenesis of type 2 diabetes, but nothing is known about lncRNA expression changes of lymphatic endothelial cells in response to type 2 diabetes. Methods: The GSE38396 dataset was downloaded from the Gene Expression Omnibus database and the probe sets of Human Gnome U133 Plus2.0 microarray were annotated for lncRNA. Differentially expressed lncRNAs between diabetic and non-diabetic lymphatic endothelial cells were calculated. Results: Compared with lymphatic endothelial cells in non-diabetic patients, 31 lncRNAs were downregulated and 79 lncRNAs were up-regualted in lymphatic endothelial cells of type 2 diabetic patients. Several known lncRNAs were found, such as H19, GAS5, UCA1, CRNDE, GAS5, and LINC00312. Co-expression network of differentially expressed lncRNAs and mRNAs were constructed. Based on genomic regions of these lncRNAs, we found that binding sites of MAF and TCF3 were enriched and these lncRNAs may be related to insulin reporter signaling pathway and response to insulin stimulus. Conclusions: In a word, we found a set of lncRNAs were differentially expressed in lymphatic endothelial cells in response to type 2 diabetes and these lncRNAs may be involved in the pathogenesis of diabetes-related complications. (C) 2017 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:466 / 474
页数:9
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