Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/355317
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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampBarbaro, Natália Ruggeri-
dc.contributor.authorunicampMoreno Junior, Heitor-
dc.typeArtigopt_BR
dc.titleImmune activation caused by vascular oxidation promotes fibrosis and hypertensionpt_BR
dc.contributor.authorWu, Jing-
dc.contributor.authorSaleh, Mohamed A.-
dc.contributor.authorKirabo, Annet-
dc.contributor.authorItani, Hana A.-
dc.contributor.authorMontaniel, Kim Ramil C.-
dc.contributor.authorXiao, Liang-
dc.contributor.authorChen, Wei-
dc.contributor.authorMernaugh, Raymond L.-
dc.contributor.authorCai, Hua-
dc.contributor.authorBernstein, Kenneth E.-
dc.contributor.authorGoronzy, Joerg J.-
dc.contributor.authorWeyand, Cornelia M.-
dc.contributor.authorCurci, John A.-
dc.contributor.authorBarbaro, Natalia R.-
dc.contributor.authorMoreno, Heitor-
dc.contributor.authorDavies, Sean S.-
dc.contributor.authorRoberts, L. Jackson-
dc.contributor.authorMadhur, Meena S.-
dc.contributor.authorHarrison, David G.-
dc.subjectHipertensãopt_BR
dc.subjectRigidez vascularpt_BR
dc.subjectArtrite reumatóidept_BR
dc.subjectDisfunção endotelialpt_BR
dc.subject.otherlanguageHypertensionpt_BR
dc.subject.otherlanguageVascular stiffnesspt_BR
dc.subject.otherlanguageArthritis, rheumatoidpt_BR
dc.subject.otherlanguageEndothelial dysfunctionpt_BR
dc.description.abstractVascular oxidative injury accompanies many common conditions associated with hypertension. In the present study, we employed mouse models with excessive vascular production of ROS (tg(sm/p22phox) mice, which overexpress the NADPH oxidase subunit p22(phox) smooth muscle, and mice with vascular-specific deletion of extracellular SOD) and have shown that these animals develop vascular collagen deposition, aortic stiffening, renal dysfunction, and hypertension with age. T cells from tg(5m/p22phox) mice produced high levels of IL-17A and IFN-gamma. Crossing tg(sm/p22phox) mice with lymphocyte-deficient Rag1(-/-) mice eliminated vascular inflammation, aortic stiffening, renal dysfunction, and hypertension; however, adoptive transfer of T cells restored these processes. Isoketal-protein adducts, which are immunogenic, were increased in aortas, DCs, and macrophages of tg(sm/P22Phox) mice. Autologous pulsing with tg(sm/p22phox) aortic homogenates promoted DCs of tg(sm/p22phox) mice to stimulate T cell proliferation and production of IFN-gamma, IL-17A, and TNF-alpha. Treatment with the superoxide scavenger tempol or the isoketal scavenger 2-hydroxybenzylamine (2-HOBA) normalized blood pressure; prevented vascular inflammation, aortic stiffening, and hypertension; and prevented DC and T cell activation. Moreover, in human aortas, the aortic content of isoketal adducts correlated with fibrosis and inflammation severity. Together, these results define a pathway linking vascular oxidant stress to immune activation and aortic stiffening and provide insight into the systemic inflammation encountered in common vascular diseasespt_BR
dc.relation.ispartofJournal of clinical investigationpt_BR
dc.relation.ispartofabbreviationJ. clin. invest.pt_BR
dc.publisher.cityAnn Arbor, MIpt_BR
dc.publisher.countryEstados Unidospt_BR
dc.publisherAmerican Society for Clinical Investigationpt_BR
dc.date.issued2016-
dc.date.monthofcirculationJan.pt_BR
dc.language.isoengpt_BR
dc.description.volume126pt_BR
dc.description.issuenumber1pt_BR
dc.description.firstpage50pt_BR
dc.description.lastpage67pt_BR
dc.rightsAbertopt_BR
dc.sourceWOSpt_BR
dc.identifier.issn0021-9738pt_BR
dc.identifier.eissn1558-8238pt_BR
dc.identifier.doi10.1172/JCI80761pt_BR
dc.identifier.doi10.1172/JCI87425pt_BR
dc.identifier.urlhttps://www.jci.org/articles/view/80761pt_BR
dc.identifier.urlhttps://www.jci.org/articles/view/87425pt_BR
dc.date.available2021-02-05T20:35:56Z-
dc.date.accessioned2021-02-05T20:35:56Z-
dc.description.provenanceSubmitted by Cintia Oliveira de Moura (cintiaom@unicamp.br) on 2021-02-05T20:35:56Z No. of bitstreams: 0en
dc.description.provenanceMade available in DSpace on 2021-02-05T20:35:56Z (GMT). No. of bitstreams: 0 Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/355317-
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Clínica Médicapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source000367765600010pt_BR
dc.identifier.source000373522300052pt_BR
dc.creator.orcid0000-0003-1596-1085pt_BR
dc.creator.orcid0000-0001-6330-697Xpt_BR
dc.type.formArtigo de pesquisapt_BR
dc.description.sponsorNoteUnited States Department of Health & Human Services; National Institutes of Health (NIH) - USA; VITA; American Heart Association; Vanderbilt Physician Scientist Development Award; NIH National Heart Lung & Blood Institute (NHLBI); NIH National Institute of Allergy & Infectious Diseases (NIAID); NIH National Institute of Arthritis & Musculoskeletal & Skin Diseases (NIAMS); NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK); NIH National Institute of General Medical Sciences (NIGMS); NIH National Institute on Aging (NIA)pt_BR
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