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CCBE1 Is Essential for Epicardial Function during Myocardium Development

2022-10-20Artigo científico Acesso aberto
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dc.contributor.authorBonet, Fernando
dc.contributor.authorAñez, Sabrina Brito
dc.contributor.authorInácio, José Manuel
dc.contributor.authorFutschik, Matthias E.
dc.contributor.authorBelo, José Antonio
dc.contributor.authorBelo, José A.
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2022-11-04T22:11:22Z
dc.date.available2022-11-04T22:11:22Z
dc.date.issued2022-10-20
dc.descriptionFunding: This work was supported by Fundação para a Ciência e a Tecnologia (FCT) grants (PTDC/MEC-CAR/29590/2017) to JA Belo and by the Scientific Employment Stimulus to JMI (Norma Transitória 8189/2018, FCT), and iNOVA4Health—UIDB/Multi/04462/2013, a program Int. J. Mol. Sci. 2022, 23, 12642 14 of 17 financially supported by Fundação para a Ciência e Tecnologia/Ministério da Educação e Ciência, through national funds and co-funded by FEDER under the PT2020 Partnership Agreement.
dc.description.abstractThe epicardium is a single cell layer of mesothelial cells that plays a critical role during heart development contributing to different cardiac cell types of the developing heart through epithelial-to-mesenchymal transition (EMT). Moreover, the epicardium is a source of secreted growth factors that promote myocardial growth. CCBE1 is a secreted extracellular matrix protein expressed by epicardial cells that is required for the formation of the primitive coronary plexus. However, the role of CCBE1 during epicardial development was still unknown. Here, using a Ccbe1 knockout (KO) mouse model, we observed that loss of CCBE1 leads to congenital heart defects including thinner and hyper-trabeculated ventricular myocardium. In addition, Ccbe1 mutant hearts displayed reduced proliferation of cardiomyocyte and epicardial cells. Epicardial outgrowth culture assay to assess epicardial-derived cells (EPDC) migration showed reduced invasion of the collagen gel by EPDCs in Ccbe1 KO epicardial explants. Ccbe1 KO hearts also displayed fewer nonmyocyte/nonendothelial cells intramyocardially with a reduced proliferation rate. Additionally, RNA-seq data and experimental validation by qRT-PCR showed a marked deregulation of EMT-related genes in developing Ccbe1 mutant hearts. Together, these findings indicate that the myocardium defects in Ccbe1 KO mice arise from disruption of epicardial development and function.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent3948559
dc.identifier.doi10.3390/ijms232012642
dc.identifier.issn1422-0067
dc.identifier.otherPURE: 47564377
dc.identifier.otherPURE UUID: 3888234a-b403-4eb9-a270-71dc83df9df9
dc.identifier.otherScopus: 85140819391
dc.identifier.otherPubMed: 36293499
dc.identifier.otherWOS: 000873097500001
dc.identifier.urihttp://hdl.handle.net/10362/145250
dc.identifier.urlhttps://www.scopus.com/pages/publications/85140819391
dc.language.isoeng
dc.peerreviewedyes
dc.subjectCCBE1
dc.subjectEMT
dc.subjectepicardial derived cells
dc.subjectepicardium
dc.subjectheart development
dc.subjectmyocardial growth
dc.subjectCatalysis
dc.subjectMolecular Biology
dc.subjectSpectroscopy
dc.subjectComputer Science Applications
dc.subjectPhysical and Theoretical Chemistry
dc.subjectOrganic Chemistry
dc.subjectInorganic Chemistry
dc.titleCCBE1 Is Essential for Epicardial Function during Myocardium Developmenten
dc.typejournal article
degois.publication.issue20
degois.publication.titleInternational Journal of Molecular Sciences
degois.publication.volume23
dspace.entity.typePublication
person.familyNameBelo
person.givenNameJosé A.
person.identifier.ciencia-idBF13-08E9-25E6
person.identifier.orcid0000-0001-7384-0949
person.identifier.ridF-4444-2012
person.identifier.scopus-author-id6602141392
rcaap.rightsopenAccess
relation.isAuthorOfPublication9f75224c-9cf2-478f-9c7c-d22527950642
relation.isAuthorOfPublication.latestForDiscovery9f75224c-9cf2-478f-9c7c-d22527950642

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