The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells
Abstract Background Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis...
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doaj-318179084cb3468dbf708cbb7597283a2020-11-24T21:59:51ZengBMCBMC Genomics1471-21642018-06-0119111210.1186/s12864-018-4876-6The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cellsJohannes Rainer0Viviana Meraviglia1Hagen Blankenburg2Chiara Piubelli3Peter P. Pramstaller4Adolfo Paolin5Elisa Cogliati6Giulio Pompilio7Elena Sommariva8Francisco S. Domingues9Alessandra Rossini10Institute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckTreviso Tissue Bank FoundationTreviso Tissue Bank FoundationVascular Biology and Regenerative Medicine UnitVascular Biology and Regenerative Medicine UnitInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckInstitute for Biomedicine, Eurac Research, Affiliated Institute of the University of LübeckAbstract Background Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification. Results We identified 3 miRNAs and 272 genes as significantly differentially expressed at a 5% false discovery rate. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion-related biological processes. Functional similarity and protein interaction-based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling. Conclusions We determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs, specifically miR-29b-3p, to ACM pathogenesis or phenotype maintenance.http://link.springer.com/article/10.1186/s12864-018-4876-6Arrhythmogenic cardiomyopathyCardiac stromal cellsmicroRNA expressionGene expressionGenomicsTranscriptome profiling |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Johannes Rainer Viviana Meraviglia Hagen Blankenburg Chiara Piubelli Peter P. Pramstaller Adolfo Paolin Elisa Cogliati Giulio Pompilio Elena Sommariva Francisco S. Domingues Alessandra Rossini |
spellingShingle |
Johannes Rainer Viviana Meraviglia Hagen Blankenburg Chiara Piubelli Peter P. Pramstaller Adolfo Paolin Elisa Cogliati Giulio Pompilio Elena Sommariva Francisco S. Domingues Alessandra Rossini The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells BMC Genomics Arrhythmogenic cardiomyopathy Cardiac stromal cells microRNA expression Gene expression Genomics Transcriptome profiling |
author_facet |
Johannes Rainer Viviana Meraviglia Hagen Blankenburg Chiara Piubelli Peter P. Pramstaller Adolfo Paolin Elisa Cogliati Giulio Pompilio Elena Sommariva Francisco S. Domingues Alessandra Rossini |
author_sort |
Johannes Rainer |
title |
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells |
title_short |
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells |
title_full |
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells |
title_fullStr |
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells |
title_full_unstemmed |
The arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells |
title_sort |
arrhythmogenic cardiomyopathy-specific coding and non-coding transcriptome in human cardiac stromal cells |
publisher |
BMC |
series |
BMC Genomics |
issn |
1471-2164 |
publishDate |
2018-06-01 |
description |
Abstract Background Arrhythmogenic cardiomyopathy (ACM) is a genetic autosomal disease characterized by abnormal cell-cell adhesion, cardiomyocyte death, progressive fibro-adipose replacement of the myocardium, arrhythmias and sudden death. Several different cell types contribute to the pathogenesis of ACM, including, as recently described, cardiac stromal cells (CStCs). In the present study, we aim to identify ACM-specific expression profiles of human CStCs derived from endomyocardial biopsies of ACM patients and healthy individuals employing TaqMan Low Density Arrays for miRNA expression profiling, and high throughput sequencing for gene expression quantification. Results We identified 3 miRNAs and 272 genes as significantly differentially expressed at a 5% false discovery rate. Both the differentially expressed genes as well as the target genes of the ACM-specific miRNAs were found to be enriched in cell adhesion-related biological processes. Functional similarity and protein interaction-based network analyses performed on the identified deregulated genes, miRNA targets and known ACM-causative genes revealed clusters of highly related genes involved in cell adhesion, extracellular matrix organization, lipid transport and ephrin receptor signaling. Conclusions We determined for the first time the coding and non-coding transcriptome characteristic of ACM cardiac stromal cells, finding evidence for a potential contribution of miRNAs, specifically miR-29b-3p, to ACM pathogenesis or phenotype maintenance. |
topic |
Arrhythmogenic cardiomyopathy Cardiac stromal cells microRNA expression Gene expression Genomics Transcriptome profiling |
url |
http://link.springer.com/article/10.1186/s12864-018-4876-6 |
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