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dc.creatorRocio García De la Garza
dc.creatorGabriel Amador Aguirre
dc.creatorIrene Martín Del Estal
dc.creatorMariano García-Magariño Alonso
dc.creatorMaría Inmaculada Castilla de Cortázar Larrea
dc.creatorVíctor Javier Lara Díaz
dc.creatorLuis Alonso Morales Garza
dc.date2017
dc.date.accessioned2018-10-18T21:51:02Z
dc.date.available2018-10-18T21:51:02Z
dc.identifier.issn11387548
dc.identifier.doi10.1007/s13105-016-0545-x
dc.identifier.urihttp://hdl.handle.net/11285/630492
dc.descriptionEven though the liver synthesizes most of circulating IGF-1, it lacks its receptor under physiological conditions. However, according to previous studies, a damaged liver expresses the receptor. For this reason, herein, we examine hepatic histology and expression of genes encoding proteins of the cytoskeleton, extracellular matrix, and cell-cell molecules and inflammation-related proteins. A partial IGF-1 deficiency murine model was used to investigate IGF-1’s effects on liver by comparing wild-type controls, heterozygous igf1+/−, and heterozygous mice treated with IGF-1 for 10 days. Histology, microarray for mRNA gene expression, RT-qPCR, and lipid peroxidation were assessed. Microarray analyses revealed significant underexpression of igf1 in heterozygous mice compared to control mice, restoring normal liver expression after treatment, which then normalized its circulating levels. IGF-1 receptor mRNA was overexpressed in Hz mice liver, while treated mice displayed a similar expression to that of the controls. Heterozygous mice showed overexpression of several genes encoding proteins related to inflammatory and acute-phase proteins and underexpression or overexpression of genes which coded for extracellular matrix, cytoskeleton, and cell junction components. Histology revealed an altered hepatic architecture. In addition, liver oxidative damage was found increased in the heterozygous group. The mere IGF-1 partial deficiency is associated with relevant alterations of the hepatic architecture and expression of genes involved in cytoskeleton, hepatocyte polarity, cell junctions, and extracellular matrix proteins. Moreover, it induces hepatic expression of the IGF-1 receptor and elevated acute-phase and inflammation mediators, which all resulted in liver oxidative damage. © 2017, The Author(s).
dc.languageeng
dc.publisherSpringer Netherlands
dc.relationhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85010767221&doi=10.1007%2fs13105-016-0545-x&partnerID=40&md5=66c86dd8b523a7d4cfa677705cf79c84
dc.relationInvestigadores
dc.relationEstudiantes
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0
dc.sourceJournal of Physiology and Biochemistry
dc.subjectacute phase protein
dc.subjectautacoid
dc.subjectlipid
dc.subjectmessenger RNA
dc.subjectscleroprotein
dc.subjectsomatomedin C
dc.subjectacute phase protein
dc.subjectautacoid
dc.subjectcadherin
dc.subjectcytoskeleton protein
dc.subjectinsulin-like growth factor-1, mouse
dc.subjectscleroprotein
dc.subjectsomatomedin C
dc.subjectsomatomedin receptor
dc.subjecttight junction protein
dc.subjectacute phase response
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcell junction
dc.subjectcell polarity
dc.subjectcontrolled study
dc.subjectcytoskeleton
dc.subjectextracellular matrix
dc.subjectgene expression regulation
dc.subjectgene overexpression
dc.subjectheterozygosity
dc.subjecthistology
dc.subjectigf1 gene
dc.subjectinflammation
dc.subjectlipid peroxidation
dc.subjectliver structure
dc.subjectliver tissue
dc.subjectmale
dc.subjectmicroarray analysis
dc.subjectmouse
dc.subjectmurine model
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectprotein analysis
dc.subjectprotein blood level
dc.subjectprotein deficiency
dc.subjectprotein function
dc.subjectreverse transcription polymerase chain reaction
dc.subjectwild type
dc.subjectanimal
dc.subjectcomparative study
dc.subjectcross breeding
dc.subjectdesmosome
dc.subjectgene expression profiling
dc.subjectgenetics
dc.subjecthepatitis
dc.subjectimmunology
dc.subjectliver
dc.subjectmetabolism
dc.subjectpathology
dc.subjectsubcutaneous drug administration
dc.subjecttransgenic mouse
dc.subjectAcute-Phase Proteins
dc.subjectAnimals
dc.subjectCadherins
dc.subjectCrosses, Genetic
dc.subjectCytoskeletal Proteins
dc.subjectDesmosomes
dc.subjectExtracellular Matrix Proteins
dc.subjectGene Expression Profiling
dc.subjectGene Expression Regulation
dc.subjectHepatitis
dc.subjectInflammation Mediators
dc.subjectInjections, Subcutaneous
dc.subjectInsulin-Like Growth Factor I
dc.subjectLipid Peroxidation
dc.subjectLiver
dc.subjectMale
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectOxidative Stress
dc.subjectReceptors, Somatomedin
dc.subjectTight Junction Proteins
dc.subject.classification7 INGENIERÍA Y TECNOLOGÍA
dc.titleIGF-1 modulates gene expression of proteins involved in inflammation, cytoskeleton, and liver architecture
dc.typeArtículo
dc.identifier.volume73
dc.identifier.issue2
dc.identifier.startpage245
dc.identifier.endpage258
refterms.dateFOA2018-10-18T21:51:02Z


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