Analysis of long non-coding RNA expression profiles in high-glucose treated vascular endothelial cells

BMC Endocrine Disorders

Guoxi Jin¹  Langen Zhuang¹  Xiaoyan Pei¹  Xiaolei Hu¹  Xiaoli Li¹  Qiong Wang¹  Erqin Xu² 

[1] Department of Endocrinology, First Affiliated Hospital of Bengbu Medical College;Room of Physical Diagnostics, Clinical College of Medicine, Bengbu Medical College;

关键词: lncRNA;    Diabetes mellitus;    HUVECs;    Expression profiling;    Hyperglycemia;    RNA-seq;   

DOI  :  10.1186/s12902-020-00593-6

来源: DOAJ

【 摘 要 】

Abstract Background Diabetes mellitus is often associated with microvascular and macrovascular lesions, and hyperglycemia-induced vascular endothelial cell damage is a key factor. Methods We investigated long non-coding RNAs (lncRNAs) and mRNAs that are affected by hyperglycemia-induced damage using human umbilical vein endothelial cells (HUVECs) as a model. HUVECs were cultured under high (25 mmol/L) or normal (5 mmol/L) glucose conditions for 6 d, and then lncRNAs and protein-coding transcripts were profiled by RNA-seq. Result Among 40,379 lncRNAs screened, 214 were upregulated (log2 [fold-change] > 1, FDR < 0.05) and 197 were downregulated (log2 [fold-change] < − 1, FDR < 0.05) in response to high-glucose. Furthermore, among 28,431 protein-coding genes screened, 778 were upregulated and 998 were downregulated. A total of 945 lncRNA/mRNA pairs were identified, including 126 differentially expressed lncRNAs predicted to target 201 mRNAs, among which 26 were cis-regulatory interactions. The corresponding lncRNA-mRNA network was composed of 354 lncRNA nodes, 1167 mRNA nodes and 9735 edges. Dozens of lncRNAs with high degree may play important roles in high-glucose-induced HUVEC damage, including ENST00000600527, NONHSAT037576.2, NONHSAT135706.2, ENST00000602127, NONHSAT200243.1, NONHSAT217282.1, NONHSAT176260.1, NONHSAT199075.1, NONHSAT067063.2, NONHSAT058417.2. Conclusion These observations may provide novel insights into the regulatory molecules and pathways of hyperglycemia-related endothelial dysfunction in diabetes-associated vascular disease.

【 授权许可】

Unknown