Cell therapy prevents structural, functional and molecular remodeling of remote non-infarcted myocardium

dc.creatordos Santos, L
dc.creatorGoncalves, GA
dc.creatorDavel, AP
dc.creatorSantos, AA
dc.creatorKrieger, JE
dc.creatorRossoni, LV
dc.creatorTucci, PJF
dc.date2013
dc.dateOCT 9
dc.date2014-08-01T18:24:54Z
dc.date2015-11-26T17:03:51Z
dc.date2014-08-01T18:24:54Z
dc.date2015-11-26T17:03:51Z
dc.date.accessioned2018-03-28T23:52:03Z
dc.date.available2018-03-28T23:52:03Z
dc.identifierInternational Journal Of Cardiology. Elsevier Ireland Ltd, v. 168, n. 4, n. 3829, n. 3836, 2013.
dc.identifier0167-5273
dc.identifier1874-1754
dc.identifierWOS:000326219600112
dc.identifier10.1016/j.ijcard.2013.06.026
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/78567
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/78567
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1279196
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionBackground/objectives: Therapy using bone marrow (BM) cells has been tested experimentally and clinically due to the potential ability to restore cardiac function by regenerating lost myocytes or increasing the survival of tissues at risk after myocardial infarction (MI). In this study we aimed to evaluate whether BM-derived mononuclear cell (MNC) implantation can positively influence the post-MI structural remodeling, contractility and Ca(2+)-handling proteins of the remote non-infarcted tissue in rats. Methods and results: After 48 h of MI induction, saline or BM-MNC were injected. Six weeks later, MI scars were slightly smaller and thicker, and cardiac dilatation was just partially prevented by cell therapy. However, the cardiac performance under hemodynamic stress was totally preserved in the BM-MNC treated group if compared to the untreated group, associated with normal contractility of remote myocardium as analyzed in vitro. The impaired post-rest potentiation of contractile force, associated with decreased protein expression of the sarcoplasmic reticulum Ca2+-ATPase and phosphorylated-phospholamban and overexpression of Na(+)/Ca(2+) exchanger, were prevented by BM-MNC, indicating preservation of the Ca(2+) handling. Finally, pathological changes on remodeled remote tissue such as myocyte hypertrophy, interstitial fibrosis and capillary rarefaction were also mitigated by cell therapy. Conclusions: BM-MNC therapy was able to prevent cardiac structural and molecular remodeling after MI, avoiding pathological changes on Ca(2+)-handling proteins and preserving contractile behavior of the viable myocardium, which could be the major contributor to the improvements of global cardiac performance after cell transplantation despite that scar tissue still exists. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
dc.description168
dc.description4
dc.description3829
dc.description3836
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageen
dc.publisherElsevier Ireland Ltd
dc.publisherClare
dc.publisherIrlanda
dc.relationInternational Journal Of Cardiology
dc.relationInt. J. Cardiol.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectMyocardial remodeling
dc.subjectStem-cell
dc.subjectCalcium-handling
dc.subjectCapillary
dc.subjectHypertrophy
dc.subjectMesenchymal Stem-cells
dc.subjectImprove Cardiac-function
dc.subjectHeart-failure
dc.subjectIschemic-heart
dc.subjectRat Model
dc.subjectInfarction
dc.subjectTransplantation
dc.subjectSize
dc.subjectPerformance
dc.subjectInjection
dc.titleCell therapy prevents structural, functional and molecular remodeling of remote non-infarcted myocardium
dc.typeArtículos de revistas


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