Partial IGF-1 deficiency is sufficient to reduce heart contractibility, angiotensin II sensibility, and alter gene expression of structural and functional cardiac proteins

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dc.creatorGabriel Amador Aguirre
dc.creatorIrene Martín Del Estal
dc.creatorMaría Inmaculada Castilla de Cortázar Larrea
dc.creatorJosé Luis González Guerra
dc.date2017
dc.date.accessioned2018-10-18T21:21:56Z
dc.date.available2018-10-18T21:21:56Z
dc.descriptionCirculating levels of IGF-1 may decrease under several circumstances like ageing, metabolic syndrome, and advanced cirrhosis. This reduction is associated with insulin resistance, dyslipidemia, progression to type 2 diabetes, and increased risk for cardiovascular diseases. However, underlying mechanisms between IGF-1 deficiency and cardiovascular disease remain elusive. The specific aim of the present work was to study whether the partial IGF-1 deficiency influences heart and/or coronary circulation, comparing vasoactive factors before and after of ischemia-reperfusion (I/R). In addition, histology of the heart was performed together with cardiac gene expression for proteins involved in structure and function (extracellular matrix, contractile proteins, active peptides); carried out using microarrays, followed by RT-qPCR confirmation of the three experimental groups. IGF-1 partial deficiency is associated to a reduction in contractility and angiotensin II sensitivity, interstitial fibrosis as well as altered expression pattern of genes involved in extracellular matrix proteins, calcium dynamics, and cardiac structure and function. Although this work is descriptive, it provides a clear insight of the impact that partial IGF-1 deficiency on the heart and establishes this experimental model as suitable for studying cardiac disease mechanisms and exploring therapeutic options for patients under IGF-1 deficiency conditions. © 2017 González-Guerra et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.identifier.doi10.1371/journal.pone.0181760
dc.identifier.issn19326203
dc.identifier.issue8
dc.identifier.urihttp://hdl.handle.net/11285/630439
dc.identifier.volume12
dc.languageeng
dc.publisherPublic Library of Science
dc.relationhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85027372642&doi=10.1371%2fjournal.pone.0181760&partnerID=40&md5=5030cb63c417b116697834e1c40f4ede
dc.relationInvestigadores
dc.relationEstudiantes
dc.rights.urihttp://creativecommons.org/licenses/by/4.0
dc.sourcePLoS ONE
dc.subjectangiotensin II
dc.subjectcalcium
dc.subjectconnective tissue growth factor
dc.subjectcontractile protein
dc.subjectprotein Grem1
dc.subjectscleroprotein
dc.subjectsomatomedin B
dc.subjectsomatomedin B receptor
dc.subjectsomatomedin binding protein 1
dc.subjectsomatomedin binding protein 2
dc.subjectsomatomedin binding protein 3
dc.subjectsomatomedin binding protein 4
dc.subjectsomatomedin binding protein 5
dc.subjectsomatomedin binding protein 6
dc.subjectsomatomedin C
dc.subjectsomatomedin C receptor
dc.subjectunclassified drug
dc.subjectangiotensin II
dc.subjectbradykinin
dc.subjectsomatomedin C
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcalcium homeostasis
dc.subjectcontrolled study
dc.subjectcoronary artery blood flow
dc.subjectCtgf gene
dc.subjectextracellular matrix
dc.subjectgene
dc.subjectgene expression
dc.subjectGrem1 gene
dc.subjectheart muscle contractility
dc.subjectheart muscle fibrosis
dc.subjectheart weight
dc.subjecthistology
dc.subjectIgf1 gene
dc.subjectIgf1r gene
dc.subjectIgf2 gene
dc.subjectIgf2r gene
dc.subjectIgfbp1 gene
dc.subjectIgfbp2 gene
dc.subjectIgfbp3 gene
dc.subjectIgfbp4 gene
dc.subjectIgfbp5 gene
dc.subjectIgfbp6 gene
dc.subjectmale
dc.subjectmouse
dc.subjectnonhuman
dc.subjectprotein blood level
dc.subjectreal time polymerase chain reaction
dc.subjectregulatory mechanism
dc.subjectreperfusion injury
dc.subjectanimal
dc.subjectbody weight
dc.subjectcardiac muscle
dc.subjectdeficiency
dc.subjectdrug effects
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectheart contraction
dc.subjecthemodynamics
dc.subjectmetabolism
dc.subjectorgan size
dc.subjectpathology
dc.subjectperfusion
dc.subjecttransgenic mouse
dc.subjectvasoconstriction
dc.subjectvasodilatation
dc.subjectAngiotensin II
dc.subjectAnimals
dc.subjectBody Weight
dc.subjectBradykinin
dc.subjectExtracellular Matrix
dc.subjectGene Expression Regulation
dc.subjectHemodynamics
dc.subjectInsulin-Like Growth Factor I
dc.subjectMice, Transgenic
dc.subjectMyocardial Contraction
dc.subjectMyocardium
dc.subjectOrgan Size
dc.subjectPerfusion
dc.subjectReal-Time Polymerase Chain Reaction
dc.subjectVasoconstriction
dc.subjectVasodilation
dc.subject.classification7 INGENIERÍA Y TECNOLOGÍA
dc.titlePartial IGF-1 deficiency is sufficient to reduce heart contractibility, angiotensin II sensibility, and alter gene expression of structural and functional cardiac proteins
dc.typeArtículo
refterms.dateFOA2018-10-18T21:21:56Z

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