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Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect

Ventricular septal defects (VSD) are the most common form of congenital heart disease, which is the leading non-infectious cause of death in children; nevertheless, the exact cause of VSD is not yet fully understood. Long non-coding RNAs (lncRNAs) have been shown to play key roles in various biologi...

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Autores principales: Song, Guixian, Shen, Yahui, Zhu, Jingai, Liu, Hailang, Liu, Ming, Shen, Ya-Qing, Zhu, Shasha, Kong, Xiangqing, Yu, Zhangbin, Qian, Lingmei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3797806/
https://www.ncbi.nlm.nih.gov/pubmed/24147006
http://dx.doi.org/10.1371/journal.pone.0077492
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author Song, Guixian
Shen, Yahui
Zhu, Jingai
Liu, Hailang
Liu, Ming
Shen, Ya-Qing
Zhu, Shasha
Kong, Xiangqing
Yu, Zhangbin
Qian, Lingmei
author_facet Song, Guixian
Shen, Yahui
Zhu, Jingai
Liu, Hailang
Liu, Ming
Shen, Ya-Qing
Zhu, Shasha
Kong, Xiangqing
Yu, Zhangbin
Qian, Lingmei
author_sort Song, Guixian
collection PubMed
description Ventricular septal defects (VSD) are the most common form of congenital heart disease, which is the leading non-infectious cause of death in children; nevertheless, the exact cause of VSD is not yet fully understood. Long non-coding RNAs (lncRNAs) have been shown to play key roles in various biological processes, such as imprinting control, circuitry controlling pluripotency and differentiation, immune responses and chromosome dynamics. Notably, a growing number of lncRNAs have been implicated in disease etiology, although an association with VSD has not been reported. In the present study, we conducted an integrated analysis of dysregulated lncRNAs, focusing specifically on the identification and characterization of lncRNAs potentially involving in initiation of VSD. Comparison of the transcriptome profiles of cardiac tissues from VSD-affected and normal hearts was performed using a second-generation lncRNA microarray, which covers the vast majority of expressed RefSeq transcripts (29,241 lncRNAs and 30,215 coding transcripts). In total, 880 lncRNAs were upregulated and 628 were downregulated in VSD. Furthermore, our established filtering pipeline indicated an association of two lncRNAs, ENST00000513542 and RP11-473L15.2, with VSD. This dysregulation of the lncRNA profile provides a novel insight into the etiology of VSD and furthermore, illustrates the intricate relationship between coding and ncRNA transcripts in cardiac development. These data may offer a background/reference resource for future functional studies of lncRNAs related to VSD.
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spelling pubmed-37978062013-10-21 Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect Song, Guixian Shen, Yahui Zhu, Jingai Liu, Hailang Liu, Ming Shen, Ya-Qing Zhu, Shasha Kong, Xiangqing Yu, Zhangbin Qian, Lingmei PLoS One Research Article Ventricular septal defects (VSD) are the most common form of congenital heart disease, which is the leading non-infectious cause of death in children; nevertheless, the exact cause of VSD is not yet fully understood. Long non-coding RNAs (lncRNAs) have been shown to play key roles in various biological processes, such as imprinting control, circuitry controlling pluripotency and differentiation, immune responses and chromosome dynamics. Notably, a growing number of lncRNAs have been implicated in disease etiology, although an association with VSD has not been reported. In the present study, we conducted an integrated analysis of dysregulated lncRNAs, focusing specifically on the identification and characterization of lncRNAs potentially involving in initiation of VSD. Comparison of the transcriptome profiles of cardiac tissues from VSD-affected and normal hearts was performed using a second-generation lncRNA microarray, which covers the vast majority of expressed RefSeq transcripts (29,241 lncRNAs and 30,215 coding transcripts). In total, 880 lncRNAs were upregulated and 628 were downregulated in VSD. Furthermore, our established filtering pipeline indicated an association of two lncRNAs, ENST00000513542 and RP11-473L15.2, with VSD. This dysregulation of the lncRNA profile provides a novel insight into the etiology of VSD and furthermore, illustrates the intricate relationship between coding and ncRNA transcripts in cardiac development. These data may offer a background/reference resource for future functional studies of lncRNAs related to VSD. Public Library of Science 2013-10-16 /pmc/articles/PMC3797806/ /pubmed/24147006 http://dx.doi.org/10.1371/journal.pone.0077492 Text en © 2013 Song et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Song, Guixian
Shen, Yahui
Zhu, Jingai
Liu, Hailang
Liu, Ming
Shen, Ya-Qing
Zhu, Shasha
Kong, Xiangqing
Yu, Zhangbin
Qian, Lingmei
Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect
title Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect
title_full Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect
title_fullStr Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect
title_full_unstemmed Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect
title_short Integrated Analysis of Dysregulated lncRNA Expression in Fetal Cardiac Tissues with Ventricular Septal Defect
title_sort integrated analysis of dysregulated lncrna expression in fetal cardiac tissues with ventricular septal defect
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3797806/
https://www.ncbi.nlm.nih.gov/pubmed/24147006
http://dx.doi.org/10.1371/journal.pone.0077492
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