About: Gene Expression Networks in the Murine Pulmonary Myocardium Provide Insight into the Pathobiology of Atrial Fibrillation

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About: Gene Expression Networks in the Murine Pulmonary Myocardium Provide Insight into the Pathobiology of Atrial Fibrillation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Gene Expression Networks in the Murine Pulmonary Myocardium Provide Insight into the Pathobiology of Atrial Fibrillation
Creator	Boutilier, Jordan Henry, Peter Kenny, Jacob Mann, Tracy Morahan, Grant Dilley, Rodney Hoffman, Gary Laing, Nigel Mcnamara, Elyshia Nowak, Kristen Taylor, Rhonda
Source	Medline; PMC
abstract	The pulmonary myocardium is a muscular coat surrounding the pulmonary and caval veins. Although its definitive physiological function is unknown, it may have a pathological role as the source of ectopic beats initiating atrial fibrillation. How the pulmonary myocardium gains pacemaker function is not clearly defined, although recent evidence indicates that changed transcriptional gene expression networks are at fault. The gene expression profile of this distinct cell type in situ was examined to investigate underlying molecular events that might contribute to atrial fibrillation. Via systems genetics, a whole-lung transcriptome data set from the BXD recombinant inbred mouse resource was analyzed, uncovering a pulmonary cardiomyocyte gene network of 24 transcripts, coordinately regulated by chromosome 1 and 2 loci. Promoter enrichment analysis and interrogation of publicly available ChIP-seq data suggested that transcription of this gene network may be regulated by the concerted activity of NKX2-5, serum response factor, myocyte enhancer factor 2, and also, at a post-transcriptional level, by RNA binding protein motif 20. Gene ontology terms indicate that this gene network overlaps with molecular markers of the stressed heart. Therefore, we propose that perturbed regulation of this gene network might lead to altered calcium handling, myocyte growth, and contractile force contributing to the aberrant electrophysiological properties observed in atrial fibrillation. We reveal novel molecular interactions and pathways representing possible therapeutic targets for atrial fibrillation. In addition, we highlight the utility of recombinant inbred mouse resources in detecting and characterizing gene expression networks of relatively small populations of cells that have a pathological significance.
has issue date	2017-07-18(xsd:dateTime)
bibo:doi	10.1534/g3.117.044651
bibo:pmid	28720711
has license	cc-by
sha1sum (hex)	97f0de00cdfd52961c9a8611c306de5778556eb0
schema:url	https://doi.org/10.1534/g3.117.044651
resource representing a document's title	Gene Expression Networks in the Murine Pulmonary Myocardium Provide Insight into the Pathobiology of Atrial Fibrillation
has PubMed Central identifier	PMC5592927
has PubMed identifier	28720711
schema:publication	G3 (Bethesda)
resource representing a document's body	covid:97f0de00cdfd52961c9a8611c306de5778556eb0#body_text
is schema:about of	named entity 'ATRIAL FIBRILLATION' named entity 'myocyte' named entity 'pathological' named entity 'heart' named entity 'transcripts' named entity 'changed' named entity 'reveal' named entity 'evidence' named entity 'molecular interactions' named entity 'pulmonary' named entity 'RESOURCE' named entity 'TRANSCRIPTION' named entity 'RNA BINDING PROTEIN' named entity 'EVIDENCE' named entity 'THERAPEUTIC' named entity 'CHROMOSOME 1' named entity 'TARGETS' named entity 'ELECTROPHYSIOLOGICAL PROPERTIES' named entity 'FORCE' named entity 'KEYWORDS' named entity 'MOLECULAR INTERACTIONS' named entity 'MYOCYTE ENHANCER FACTOR 2' named entity 'NETWORKS' named entity 'CHIP-SEQ' named entity 'DEFINITIVE' named entity 'CELL TYPE' named entity 'LEAD' named entity 'UNDERLYING' named entity 'PHYSIOLOGICAL FUNCTION' named entity 'PACEMAKER' named entity 'LEVEL' named entity 'PROTEIN MOTIF' named entity 'RESOURCES' named entity 'UNCOVERING' named entity 'POST' named entity 'MYOCYTE' named entity 'ADDITION' named entity 'SIGNIFICANCE' named entity 'GENETICS' named entity 'TO INVESTIGATE' named entity 'SURROUNDING' named entity 'AVAILABLE' named entity 'REVEAL' named entity 'REGULATION' named entity 'MOUSE' named entity 'ALTERED' named entity 'ANALYZED' named entity 'ECTOPIC BEATS' named entity 'SOURCE' named entity 'TRANSCRIPTS' named entity 'CELLS' named entity 'SMALL' named entity 'CHANGED' named entity 'DEFINED' named entity 'LUNG' named entity 'HEART' named entity 'MOLECULAR' named entity 'FAULT' named entity 'TRANSCRIPTOME' named entity 'MAY HAVE' named entity 'RECENT' named entity 'DISTINCT' named entity 'EVENTS' named entity 'PULMONARY' named entity 'ABERRANT' named entity 'PATHWAYS' named entity 'CONTRIBUTE ' named entity 'GENE EXPRESSION PROFILE' named entity 'FUNCTION' named entity 'OBSERVED' named entity 'SERUM RESPONSE FACTOR'

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