Whole Transcriptome Analysis of Hypertension Induced Cardiac Injury Using Deep Sequencing

被引:12
作者
Li, Tao-Tao
Li, Xiao-Yan
Jia, Li-Xin
Zhang, Jing
Zhang, Wen-Mei
Li, Yu-Lin
Qi, Yong-Fen
Du, Jie [1 ,2 ]
机构
[1] Capital Med Univ, Beijing Anzhen Hosp, 2 Anzhen Rd, Beijing 100029, Peoples R China
[2] Beijing Inst Heart Lung & Blood Vessel Dis, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
Hypertension; Cardiac injury; Transcriptome analysis; RNA-Seq; Ubiquitin C; ANGIOTENSIN-II; RNA-SEQ; EARLY-STAGE; INFLAMMATION; P53; EXPRESSION; HEART; HYPERTROPHY; ACTIVATION; MICROARRAY;
D O I
10.1159/000438659
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Hypertension plays a critical role in the cardiac inflammation and injury. However, the mechanism of how hypertension causes the cardiac injury at a molecular level remains to be elucidated. Methods: RNA-Seq has been demonstrated to be an effective approach for transcriptome analysis, which is essential to reveal the molecular constituents of cells and tissues. In this study, we investigated the global molecular events associated with the mechanism of hypertension induced cardiac injury using RNA-Seq analysis. Results: Our results showed that totally 1,801 genes with different expression variations were identified after Ang II infusion at 1, 3 and 7 days. Go analysis showed that the top 5 high enrichment Go terms were response to stress, response to wounding, cellular component organization, cell activation and defense response. KEGG pathway analysis revealed the top 5 significantly overrepresented pathways were associated with ECM-receptor interaction, focal adhesion, protein digestion and absorption, phagosome and asthma. Moreover, protein-protein interaction network analysis indicated that ubiquitin C may play a key role in the processes of hypertension-induced cardiac injury. Conclusion: Our study provides a comprehensive understanding of the transcriptome events in hypertension-induced cardiac pathology. (C) 2016 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:670 / 682
页数:13
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