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dc.contributor.authorCaptur, Gabriella
dc.contributor.authorWilson, Robert
dc.contributor.authorBennett, Michael F.
dc.contributor.authorLuxan, Guillermo 
dc.contributor.authorNasis, Arthur
dc.contributor.authorde la Pompa, Jose Luis 
dc.contributor.authorMoon, James C.
dc.contributor.authorMohun, Timothy J.
dc.date.accessioned2017-10-30T13:15:40Z
dc.date.available2017-10-30T13:15:40Z
dc.date.issued2016
dc.identifierISI:000383723600012
dc.identifier.citationJ Anat. 2016; 229(2):314-25
dc.identifier.issn0021-8782
dc.identifier.urihttp://hdl.handle.net/20.500.12105/5206
dc.description.abstractFormation of trabeculae in the embryonic heart and the remodelling that occurs prior to birth is a conspicuous, but poorly understood, feature of vertebrate cardiogenesis. Mutations disrupting trabecular development in the mouse are frequently embryonic lethal, testifying to the importance of the trabeculae, and aberrant trabecular structure is associated with several human cardiac pathologies. Here, trabecular architecture in the developing mouse embryo has been analysed using high-resolution episcopic microscopy (HREM) and three-dimensional (3D) modelling. This study shows that at all stages from mid-gestation to birth, the ventricular trabeculae comprise a complex meshwork of myocardial strands. Such an arrangement defies conventional methods of measurement, and an approach based upon fractal algorithms has been used to provide an objective measure of trabecular complexity. The extent of trabeculation as it changes along the length of left and right ventricles has been quantified, and the changes that occur from formation of the four-chambered heart until shortly before birth have been mapped. This approach not only measures qualitative features evident from visual inspection of 3D models, but also detects subtle, consistent and regionally localised differences that distinguish each ventricle and its developmental stage. Finally, the combination of HREM imaging and fractal analysis has been applied to analyse changes in embryonic heart structure in a genetic mouse model in which trabeculation is deranged. It is shown that myocardial deletion of the Notch pathway component Mib1 (Mib1(flox/flox); cTnT-cre) results in a complex array of abnormalities affecting trabeculae and other parts of the heart.
dc.description.sponsorshipThis work was supported by funding to TJM from the Medical Research Council (U117562103); to JCM by the Higher Education Funding Council for England; to JLdlP and GL by grants SAF2010-17555 and SAF2013-45543-R from the Spanish Ministry of Economy and Competitiveness (MINECO); and to GC by a research fellowship at the University College London Biomedical Research Centre from the UK National Institutes of Health Research Cardiometabolic Programme.
dc.language.isoeng
dc.publisherWiley 
dc.type.hasVersionVoR
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCardiac embryology
dc.subjectCardiogenesis
dc.subjectDevelopmental biology
dc.subjectNon-compaction cardiomyopathy
dc.subjectVENTRICULAR NONCOMPACTION CARDIOMYOPATHY
dc.subjectRESOLUTION EPISCOPIC MICROSCOPY
dc.subjectCONDUCTION SYSTEM
dc.subjectHEART DEVELOPMENT
dc.subjectNON-COMPACTION
dc.subjectPROLIFERATION
dc.subjectARCHITECTURE
dc.subjectEXPRESSION
dc.subjectMUTATIONS
dc.titleMorphogenesis of myocardial trabeculae in the mouse embryo
dc.typejournal article
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID27020702
dc.format.volume229
dc.format.page314-325
dc.identifier.doi10.1111/joa.12465
dc.contributor.funderMedical Research Council (Reino Unido) 
dc.contributor.funderHigher Education Funding Council for England
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.contributor.funderNational Institute for Health Research (Reino Unido) 
dc.description.peerreviewed
dc.identifier.e-issn1469-7580
dc.relation.publisherversionhttps://doi.org/10.1111/joa.12465
dc.identifier.journalJournal of Anatomy
dc.repisalud.orgCNICCNIC::Grupos de investigación::Señalización Intercelular durante el Desarrollo y la Enfermedad Cardiovascular
dc.repisalud.institucionCNIC
dc.relation.projectIDMINECO/ICTI2013-2016/SAF2013-45543-Res_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución 4.0 Internacional