Renovascular hypertension: effects of mesenchymal stem cells in the contralateral hypertensive kidney in rats

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dc.contributor.authorde Oliveira-Sales, Elizabeth Barbosa [UNIFESP]
dc.contributor.authorVarela, Vanessa Araujo [UNIFESP]
dc.contributor.authorMaquigussa, Edgar [UNIFESP]
dc.contributor.authorBorges, Fernanda Teixeira [UNIFESP]
dc.contributor.authorShimoura, Caroline Gusson [UNIFESP]
dc.contributor.authorGomes, Guiomar [UNIFESP]
dc.contributor.authorCampos, Ruy Ribeiro [UNIFESP]
dc.contributor.authorBoim, Mirian Aparecida [UNIFESP]
dc.date.accessioned2019-01-21T10:29:45Z
dc.date.available2019-01-21T10:29:45Z
dc.date.issued2016
dc.description.abstractMesenchymal stem cells (MSC) induced neovascularization and improved renal morphology of the stenotic kidney in 2 kidneys-1 clip (2K-1C) model of renovascular hypertension. The present study evaluated the effects of MSC in the contralateral hypertensive kidney. Three weeks after left renal artery occlusion, MSC were injected into the tail vein of the 2K-1C rats. Renal function and morphology were analyzed in both kidneys. Labeled MSC were found in stenotic and contralateral kidneys. Hypertensive 2K-1C animals presented increased circulating levels of Angiotensin II (Ang II) and renin. MSC prevented the progressive increase of blood pressure and reduced circulating Ang II and renin levels. Stenotic kidney showed reduced renal plasma flow (RPF) and glomerular filtration rate (GFR), whereas the contralateral kidney had a tendency (p > 0.5) of reduction in GFR in spite of unchanged RPF. MSC treatment caused an improvement in GFR with no effect of on RPF in the stenotic kidney. Contralateral kidney showed increased diuresis and natriuresis that were even higher in MSC-treated animals, indicating that cell treatment improved the capacity of the contralateral kidney to excrete sodium. Contralateral kidney expressed higher levels of inflammatory cytokines (IL-6, TNF-) and signs of fibrosis, which were attenuated by MSC treatment. MSC treatment improved the stenotic kidney function, and it was also beneficial to the contralateral hypertensive kidney because it improved the morphology and preserved its capacity to excrete sodium.en
dc.description.affiliationUniv Fed Sao Paulo, Div Renal, Dept Med, Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Dept Physiol, Sao Paulo, Brazil
dc.description.affiliationUnifespDept Med, Div Renal, Rua Pedro de Toledo,781-13 Floor, BR-04039032 Vila Clementino Sao Paul, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Physiol, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Nivel Superior (CAPES)
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.format.extent586-593
dc.identifierhttps://doi.org/10.3109/10641963.2016.1174253
dc.identifier.citationClinical And Experimental Hypertension. Philadelphia, v. 38, n. 7, p. 586-593, 2016.
dc.identifier.doi10.3109/10641963.2016.1174253
dc.identifier.issn1064-1963
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/49374
dc.identifier.wosWOS:000386114700004
dc.language.isoeng
dc.publisherHospital Clinicas, Univ Sao Paulo
dc.relation.ispartofClinical And Experimental Hypertension
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectMesenchymal Stem Cellsen
dc.subjectRenovascular Hypertensionen
dc.subjectRenal Functionen
dc.subjectRenin-Angiotensin SystemRenal-Artery Stenosisen
dc.subjectEndothelial Progenitor Cellsen
dc.subjectGoldblatt Hypertensionen
dc.subjectOxidative Stressen
dc.subjectBlood-Pressureen
dc.subjectMechanismsen
dc.subjectIschemiaen
dc.subject2-Kidneyen
dc.subjectInjuryen
dc.subjectRevascularizationen
dc.titleRenovascular hypertension: effects of mesenchymal stem cells in the contralateral hypertensive kidney in ratsen
dc.typeinfo:eu-repo/semantics/article
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