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Endothelial aquaporins and hypomethylation potential implications for atherosclerosis and cardiovascular disease

2018-01-01Artigo científico Acesso aberto
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dc.contributor.authorSilva, Inês Vieira da
dc.contributor.authorBarroso, Madalena
dc.contributor.authorMoura, Teresa
dc.contributor.authorCastro, Rita
dc.contributor.authorSoveral, Graça
dc.contributor.institutionDQ - Departamento de Química
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2019-07-03T22:42:17Z
dc.date.available2019-07-03T22:42:17Z
dc.date.issued2018-01-01
dc.descriptionWe thank Fundacao para a Ciencia e Tecnologia, Portugal, for financial support through the project grants PTDC/SAU-ORG/112683/2009 and UID/DTP/04138/2013 (iMed.ULisboa) and PhD fellowships PD/BD/113634/2015 (Ines Vieira da Silva) and SFRH/BD/73021/2010 (Madalena Barroso).
dc.description.abstractAquaporins (AQPs) are transmembrane channels that facilitate water and glycerol permeation through cell membranes. Recently, the water channel AQP1 was suggested to contribute to endothelial homeostasis and cardiovascular health. Less is known about endothelial aquaglyceroporins expression and its implication in cardiovascular disease (CVD). We have previously used cultured human endothelial cells under a hypomethylating environment to study endothelial dysfunction and activation, a phenotype implicated in the establishment of atherosclerosis and CVD. Here, we used the same cell model to investigate aquaporin’s expression and function in healthy or pro-atherogenic phenotype. We first confirmed key features of endothelium dysfunction and activation in our cell model, including an augmented endothelial transmigration under hypomethylation. Subsequently, we found AQP1 and AQP3 to be the most predominant AQPs accounting for water and glycerol fluxes, respectively, in the healthy endothelium. Moreover, endothelial hypomethylation led to decreased levels of AQP1 and impaired water permeability without affecting AQP3 and glycerol permeability. Furthermore, TNF-α treatment-induced AQP1 downregulation suggesting that the inflammatory NF-κB signaling pathway mediates AQP1 transcriptional repression in a pro-atherogenic endothelium, a possibility that warrants further investigation. In conclusion, our results add further support to AQP1 as a candidate player in the setting of endothelial dysfunction and CVD.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent1332894
dc.identifier.doi10.3390/ijms19010130
dc.identifier.issn1661-6596
dc.identifier.otherPURE: 13347825
dc.identifier.otherPURE UUID: 9b2f5061-ae01-4465-925b-71a11a630ef3
dc.identifier.otherScopus: 85041828153
dc.identifier.otherPubMed: 29301341
dc.identifier.otherPubMedCentral: PMC5796079
dc.identifier.otherWOS: 000424407200127
dc.identifier.urihttp://www.scopus.com/inward/record.url?scp=85041828153&partnerID=8YFLogxK
dc.identifier.urlhttps://www.scopus.com/pages/publications/85041828153
dc.language.isoeng
dc.peerreviewedyes
dc.relationinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/112683/PT
dc.relationS-Adenosyl homocysteine, non-histone protein hypomethylation, and vascular disease: another brick in the wall?
dc.relationIMPACT OF S-ADENOSYL HOMOCYSTEINE ON ENDOTHELIAL HOMEOSTASIS: POTENTIAL ROLE OF PI3K/AKT/FOXO SIGNALLING PATHWAYS
dc.subjectAquaporins
dc.subjectEndothelial dysfunction
dc.subjectHypomethylation
dc.subjectS-adenosylhomocysteine
dc.subjectWater and glycerol permeability
dc.subjectCatalysis
dc.subjectMolecular Biology
dc.subjectSpectroscopy
dc.subjectComputer Science Applications
dc.subjectPhysical and Theoretical Chemistry
dc.subjectOrganic Chemistry
dc.subjectInorganic Chemistry
dc.subjectSDG 3 - Good Health and Well-being
dc.titleEndothelial aquaporins and hypomethylation potential implications for atherosclerosis and cardiovascular diseaseen
dc.typejournal article
degois.publication.issue1
degois.publication.titleInternational Journal of Molecular Sciences
degois.publication.volume19
dspace.entity.typePublication
oaire.awardNumberPTDC/SAU-ORG/112683/2009
oaire.awardNumberUID/DTP/04138/2013
oaire.awardNumberSFRH/BD/73021/2010
oaire.awardTitleS-Adenosyl homocysteine, non-histone protein hypomethylation, and vascular disease: another brick in the wall?
oaire.awardTitleIMPACT OF S-ADENOSYL HOMOCYSTEINE ON ENDOTHELIAL HOMEOSTASIS: POTENTIAL ROLE OF PI3K/AKT/FOXO SIGNALLING PATHWAYS
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-ORG%2F112683%2F2009/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FDTP%2F04138%2F2013/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F73021%2F2010/PT
oaire.fundingStream3599-PPCDT
oaire.fundingStream5876
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccess
relation.isProjectOfPublicationaef05693-4b00-4cd2-b35a-d4000723acb8
relation.isProjectOfPublication75408fc3-18ba-471e-b265-9e62704763fd
relation.isProjectOfPublicationb02993eb-4e0a-4c6c-99ef-5c6ed4edb3a1
relation.isProjectOfPublication.latestForDiscovery75408fc3-18ba-471e-b265-9e62704763fd

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