The expression profile analysis of NKX2-5 knock-out embryonic mice to explore the pathogenesis of congenital heart disease

Abstract Background Mutation of NKX2-5 could lead to the development of congenital heart disease (CHD) which is a common inherited disease. This study aimed to investigate the pathogenesis of CHD in NKX2-5 knock-out embryonic mice. Methods The expression profile in the NKX2-5 knock-out embryonic mic...

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Bibliographic Details
Published in:Journal of cardiology 2015-12, Vol.66 (6), p.527-531
Main Authors: Li, Jian, MD, Cao, Yinyin, MD, Wu, Yao, MD, Chen, Weicheng, MD, Yuan, Yuan, MD, Ma, Xiaojing, MD, Huang, Guoying, MD
Format: Article
Language:English
Subjects:
Animals
Cardiovascular
Congenital heart disease
Differentially expressed genes
Down-Regulation
Embryonic mice
Gene Expression
Gene Expression Profiling
Gene Regulatory Networks - genetics
Heart Defects, Congenital - genetics
Homeobox Protein Nkx-2.5
Homeodomain Proteins
Latent pathways
Mice
Mice, Knockout
Regulation factors
Transcription Factors - metabolism
Up-Regulation
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Summary:Abstract Background Mutation of NKX2-5 could lead to the development of congenital heart disease (CHD) which is a common inherited disease. This study aimed to investigate the pathogenesis of CHD in NKX2-5 knock-out embryonic mice. Methods The expression profile in the NKX2-5 knock-out embryonic mice (GSE528) was downloaded from Gene Expression Omnibus. The heart tissues from the null/heterozygous embryonic day 12.5 mice were compared with wild-type mice to identify differentially expressed genes (DEGs), and then DEGs corresponding to the transcriptional factors were filtered out based on the information in the TRANSFAC database. In addition, a transcriptional regulatory network was constructed according to transcription factor binding site information from the University of California Santa Cruz database. A pathway interaction network was constructed by latent pathways identification analysis. Results The 42 DEGs corresponding to transcriptional factors from the null and heterozygous embryos were identified. The transcriptional regulatory networks included five down-regulated DEGs ( SP1 , SRY , JUND , STAT6 , and GATA6 ), and six up-regulated DEGs [ POU2F1 , NFY ( NFYA / NFYB / NFYC ), USF2 and MAX ]. Latent pathways analysis demonstrated that ribosome, glycolysis/gluconeogenesis, and dilated cardiomyopathy pathways significantly interacted. Conclusion The identified DEGs and latent pathways could provide new comprehensive view for understanding the pathogenesis of CHD.
ISSN:0914-5087
1876-4738
DOI:10.1016/j.jjcc.2014.12.022