Alamandine attenuates arterial remodelling induced by transverse aortic constriction in mice

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorSOUZA-NETO, Fernando Pedro de
dc.contributor.authorSILVA, Mario de Morais e
dc.contributor.authorSANTUCHI, Melissa de Carvalho
dc.contributor.authorALCANTARA-LEONIDIO, Thais Cristina de
dc.contributor.authorMOTTA-SANTOS, Daisy
dc.contributor.authorOLIVEIRA, Aline Cristina
dc.contributor.authorMELO, Marcos Barrouin
dc.contributor.authorCANTA, Giovanni Naves
dc.contributor.authorSOUZA, Leandro Eziquiel de
dc.contributor.authorIRIGOYEN, Maria Claudia Costa
dc.contributor.authorCAMPAGNOLE-SANTOS, Maria Jose
dc.contributor.authorGUATIMOSIM, Silvia
dc.contributor.authorSANTOS, Robson Augusto Souza
dc.contributor.authorSILVA, Rafaela Fernandes da
dc.date.accessioned2019-05-30T13:46:23Z
dc.date.available2019-05-30T13:46:23Z
dc.date.issued2019
dc.description.abstractAims: The renin-angiotensin system (RAS) plays an important role in the pathophysiology of vascular diseases, especially as a mediator of inflammation and tissue remodelling. Alamandine (Ala(1)-angiotensin-(1-7)) is a new biologically active peptide from the RAS, interacting withMas-related G-protein-coupled receptor member D. Although a growing number of studies reveal the cardioprotective effects of alamandine, there is a paucity of data on its participation in vascular remodelling associated events. In the present study, we investigated the effects of alamandine on ascending aorta remodelling after transverse aortic constriction (TAC) in mice. Methods and results: C57BL/6J male mice were divided into the following groups: Sham (sham-operated), TAC (operated) and TAC+ALA (operated and treated with alamandine-HP beta CD (2-Hydroxypropyl-beta-cyclodextrin), 30 mu g/kg/day, by gavage). Oral administration of alamandine for 14 days attenuated arterial remodelling by decreasing ascending aorta media layer thickness and the cells density in the adventitia induced by TAC. Alamandine administration attenuated ascending aorta fibrosis induced by TAC, through a reduction in the following parameters; total collagen deposition, expression collagen III and transforming growth factor-beta (TGF-beta) transcripts, matrix metalloproteinases (MMPs) activity and vascular expression of MMP-2. Importantly, alamandine decreased vascular expression of proinflammatory genes as CCL2, tumour necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta), and was able to increase expression of MRC1 and FIZZ1, pro-resolution markers, after TAC surgery. Conclusion: Alamandine treatment attenuates vascular remodelling after TAC, at least in part, through anti-fibrotic and anti-inflammatory effects. Hence, this work opens new avenues for the use of this heptapeptide also as a therapeutic target for vascular disease.eng
dc.description.indexMEDLINEeng
dc.description.sponsorshipFundacao de Apoio a Pesquisa do Estado de Minas Gerais (FAPEMIG)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Cientifico e Tecnologico/Brazil (CNPq)
dc.description.sponsorshipCoordenacao de Aperfeicoamentode Pessoal de Nivel Superior (CAPES)
dc.description.sponsorshipINCT NanoBiofar
dc.identifier.citationCLINICAL SCIENCE, v.133, n.5, p.629-643, 2019
dc.identifier.doi10.1042/CS20180547
dc.identifier.eissn1470-8736
dc.identifier.issn0143-5221
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/31950
dc.language.isoeng
dc.publisherPORTLAND PRESS LTDeng
dc.relation.ispartofClinical Science
dc.rightsrestrictedAccesseng
dc.rights.holderCopyright PORTLAND PRESS LTDeng
dc.subject.otherrenin-angiotensin systemeng
dc.subject.otherpressure-overloadeng
dc.subject.otherroot dilationeng
dc.subject.otheraneurysmseng
dc.subject.otherreceptoreng
dc.subject.othermuscleeng
dc.subject.othermodeleng
dc.subject.otherdissectionseng
dc.subject.othersuppressioneng
dc.subject.otherexpressioneng
dc.subject.wosMedicine, Research & Experimentaleng
dc.titleAlamandine attenuates arterial remodelling induced by transverse aortic constriction in miceeng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.author.externalSOUZA-NETO, Fernando Pedro de:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalSILVA, Mario de Morais e:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalSANTUCHI, Melissa de Carvalho:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalALCANTARA-LEONIDIO, Thais Cristina de:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalMOTTA-SANTOS, Daisy:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalOLIVEIRA, Aline Cristina:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalMELO, Marcos Barrouin:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalCANTA, Giovanni Naves:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalCAMPAGNOLE-SANTOS, Maria Jose:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalGUATIMOSIM, Silvia:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalSANTOS, Robson Augusto Souza:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.author.externalSILVA, Rafaela Fernandes da:Univ Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, Brazil
hcfmusp.citation.scopus26
hcfmusp.contributor.author-fmusphcLEANDRO EZIQUIEL DE SOUZA
hcfmusp.contributor.author-fmusphcMARIA CLAUDIA COSTA IRIGOYEN
hcfmusp.description.beginpage629
hcfmusp.description.endpage643
hcfmusp.description.issue5
hcfmusp.description.volume133
hcfmusp.origemWOS
hcfmusp.origem.pubmed30737255
hcfmusp.origem.scopus2-s2.0-85065064646
hcfmusp.origem.wosWOS:000462241000002
hcfmusp.publisher.cityLONDONeng
hcfmusp.publisher.countryENGLANDeng
hcfmusp.relation.referenceBertagnolli M, 2014, PEPTIDES, V51, P65, DOI 10.1016/j.peptides.2013.11.006eng
hcfmusp.relation.referenceBrooke BS, 2008, NEW ENGL J MED, V358, P2787, DOI 10.1056/NEJMoa0706585eng
hcfmusp.relation.referenceSantana ABC, 2014, BIOMED RES INT, DOI 10.1155/2014/914102eng
hcfmusp.relation.referenceChen J, 2011, CLIN EXP PHARMACOL P, V38, P570, DOI 10.1111/j.1440-1681.2011.05544.xeng
hcfmusp.relation.referenceDa Silva AR, 2017, EUR J CLIN INVEST, V47, P117, DOI 10.1111/eci.12708eng
hcfmusp.relation.referencedeAlmeida Angela C, 2010, J Vis Exp, DOI 10.3791/1729eng
hcfmusp.relation.referenceDu XJ, 2011, CLIN EXP PHARMACOL P, V38, P559, DOI 10.1111/j.1440-1681.2011.05558.xeng
hcfmusp.relation.referenceFaugeroux J, 2013, HYPERTENSION, V62, P203, DOI 10.1161/HYPERTENSIONAHA.111.00974eng
hcfmusp.relation.referenceFraga-Silva RA, 2015, VASC PHARMACOL, V74, P103, DOI 10.1016/j.vph.2015.08.014eng
hcfmusp.relation.referenceFrederiks WM, 2004, J HISTOCHEM CYTOCHEM, V52, P711, DOI 10.1369/jhc.4R6251.2004eng
hcfmusp.relation.referenceHabiyakare B, 2014, INT J EXP PATHOL, V95, P290, DOI 10.1111/iep.12087eng
hcfmusp.relation.referenceHekmat AS, 2017, CIRC J, V81, P405, DOI 10.1253/circj.CJ-16-0958eng
hcfmusp.relation.referenceHrenak J, 2016, INT J MOL SCI, V17, DOI 10.3390/ijms17071098eng
hcfmusp.relation.referenceHumphrey JD, 2015, CIRC RES, V116, P1448, DOI 10.1161/CIRCRESAHA.114.304936eng
hcfmusp.relation.referenceIrani K, 2001, CIRC RES, V88, P858, DOI 10.1161/hh0901.091205eng
hcfmusp.relation.referenceKuang SQ, 2013, ARTERIOSCL THROM VAS, V33, P2172, DOI 10.1161/ATVBAHA.113.301624eng
hcfmusp.relation.referenceLautner RQ, 2013, CIRC RES, V112, P1104, DOI 10.1161/CIRCRESAHA.113.301077eng
hcfmusp.relation.referenceLi JZ, 2013, CARDIOL CLIN, V31, P493, DOI [10.1016/j.ccl.2013.07.011, 10.1016/j.cc1.2013.07.011]eng
hcfmusp.relation.referenceLi P, 2018, LIFE SCI, V206, P106, DOI 10.1016/j.lfs.2018.04.010eng
hcfmusp.relation.referenceLiu C, 2018, AMINO ACIDS, V50, P1071, DOI 10.1007/s00726-018-2583-xeng
hcfmusp.relation.referenceLiu DG, 2016, ARTERIOSCL THROM VAS, V36, P442, DOI 10.1161/ATVBAHA.115.306861eng
hcfmusp.relation.referenceLiu Y, 2016, EUR J PHARMACOL, V791, P535, DOI 10.1016/j.ejphar.2016.07.008eng
hcfmusp.relation.referenceLu H, 2012, CLIN SCI, V123, P531, DOI 10.1042/CS20120097eng
hcfmusp.relation.referenceMagalhaes GS, 2015, BRIT J PHARMACOL, V172, P2330, DOI 10.1111/bph.13057eng
hcfmusp.relation.referenceMarques FD, 2011, HYPERTENSION, V57, P477, DOI 10.1161/HYPERTENSIONAHA.110.167346eng
hcfmusp.relation.referenceMathur D, 2016, SCI REP-UK, V6, DOI 10.1038/srep36617eng
hcfmusp.relation.referenceMilewicz DM, 2008, ANNU REV GENOM HUM G, V9, P283, DOI 10.1146/annurev.genom.8.080706.092303eng
hcfmusp.relation.referenceMoltzer E, 2011, PHARMACOL THERAPEUT, V131, P50, DOI 10.1016/j.pharmthera.2011.04.002eng
hcfmusp.relation.referenceMotta-Santos D, 2016, HYPERTENS RES, V39, P506, DOI 10.1038/hr.2016.28eng
hcfmusp.relation.referencePacurari M, 2014, INT J INFLAMM, DOI 10.1155/2014/689360eng
hcfmusp.relation.referencePage-McCaw A, 2007, NAT REV MOL CELL BIO, V8, P221, DOI 10.1038/nrm2125eng
hcfmusp.relation.referenceQaradakhi T, 2017, CARDIOVASC THER, V35, DOI 10.1111/1755-5922.12306eng
hcfmusp.relation.referenceQaradakhi T, 2016, PHARMACOL RES, V111, P820, DOI 10.1016/j.phrs.2016.07.025eng
hcfmusp.relation.referenceROCKMAN HA, 1991, P NATL ACAD SCI USA, V88, P8277, DOI 10.1073/pnas.88.18.8277eng
hcfmusp.relation.referenceSantuchi MD, 2019, MEDIAT INFLAMM, DOI 10.1155/2019/2401081eng
hcfmusp.relation.referenceSellers SL, 2018, AM J PATHOL, V188, P574, DOI 10.1016/j.ajpath.2017.11.006eng
hcfmusp.relation.referenceSongstad NT, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0089559eng
hcfmusp.relation.referenceUchiyama T, 2017, PLOS ONE, V12, DOI 10.1371/journal.pone.0178769eng
hcfmusp.relation.referenceWang XX, 2016, J MOL CELL CARDIOL, V97, P180, DOI 10.1016/j.yjmcc.2016.05.012eng
hcfmusp.relation.referenceWei H, 2012, P NATL ACAD SCI USA, V109, pE841, DOI 10.1073/pnas.1202081109eng
hcfmusp.relation.referenceXu R, 2016, PEPTIDES, V86, P85, DOI 10.1016/j.peptides.2016.10.005eng
hcfmusp.scopus.lastupdate2024-05-10
relation.isAuthorOfPublicationb273c648-931c-4157-aac9-771a86fa08dc
relation.isAuthorOfPublication124821b6-302b-4392-8a9a-b693916724e1
relation.isAuthorOfPublication.latestForDiscoveryb273c648-931c-4157-aac9-771a86fa08dc
Arquivos
Pacote Original
Agora exibindo 1 - 1 de 1
Nenhuma Miniatura disponível
Nome:
art_SOUZA-NETO_Alamandine_attenuates_arterial_remodelling_induced_by_transverse_aortic_2019.PDF
Tamanho:
1.38 MB
Formato:
Adobe Portable Document Format
Descrição:
publishedVersion (English)