Intrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial function

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dc.citation.issue6
dc.citation.volume8
dc.contributor.authorOliveira, Vanessa [UNIFESP]
dc.contributor.authorSouza, Livia Victorino de [UNIFESP]
dc.contributor.authorFernandes, Tiago
dc.contributor.authorSilva Júnior, Sebastião Donato
dc.contributor.authorCarvalho, Maria Helena Catelli de
dc.contributor.authorAkamine, Eliana Hiromi
dc.contributor.authorMichelini, Lisete Compagno
dc.contributor.authorOliveira, Edilamar Menezes de
dc.contributor.authorFranco, Maria do Carmo Pinho [UNIFESP]
dc.coverageCambridge
dc.date.accessioned2020-09-01T13:21:15Z
dc.date.available2020-09-01T13:21:15Z
dc.date.issued2017
dc.description.abstractIntrauterine growth restriction (IUGR) can induce deleterious changes in the modulatory ability of the vascular endothelium, contributing to an increased risk of developing cardiovascular diseases in the long term. However, the mechanisms involved are not fully understood. Emerging evidence has suggested the potential role of endothelial progenitor cells (EPCs) in vascular health and repair. Therefore, we aimed to evaluate the effects of IUGR on vascular reactivity and EPCs derived from the peripheral blood (PB) and bone marrow (BM) in vitro. Pregnant Wistar rats were fed an ad libitum diet (control group) or 50% of the ad libitum diet (restricted group) throughout gestation. We determined vascular reactivity, nitric oxide (NO) concentration, and endothelial nitric oxide synthase (eNOS) protein expression by evaluating the thoracic aorta of adult male offspring from both groups (aged: 19-20 weeks). Moreover, the amount, functional capacity, and senescence of EPCs were assessed in vitro. Our results indicated that IUGR reduced vasodilation via acetylcholine in aorta rings, decreased NO levels, and increased eNOS phosphorylation at Thr495. The amount of EPCs was similar between both groups; however, IUGR decreased the functional capacity of EPCs from the PB and BM. Furthermore, the senescence process was accelerated in BM-derived EPCs from IUGR rats. In summary, our findings demonstrated the deleterious changes in EPCs from IUGR rats, such as reduced EPC function and accelerated senescence in vitro. These findings may contribute towards elucidating the possible mechanisms involved in endothelial dysfunction induced by fetal programming.en
dc.description.affiliationUniv Fed Sao Paulo, Sch Med, Nephrol Div, Rua Botucatu 703, BR-04023062 Sao Paulo, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Sch Phys Educ & Sport, Biochem & Mol Biol Lab, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Inst Biomed Sci, Physiol Dept, Sao Paulo, Brazil
dc.description.affiliationUniv Sao Paulo, Inst Biomed Sci, Pharmacol Dept, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Sch Med, Nephrol Div, Rua Botucatu 703, BR-04023062 Sao Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipIDFAPESP: 2013/03139-0
dc.description.sponsorshipIDFAPESP: 2013/00311-6
dc.format.extent665-673
dc.identifierhttps://dx.doi.org/10.1017/S2040174417000484
dc.identifier.citationJournal Of Developmental Origins Of Health And Disease. Cambridge, v. 8, n. 6, p. 665-673, 2017.
dc.identifier.doi10.1017/S2040174417000484
dc.identifier.issn2040-1744
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/58151
dc.identifier.wosWOS:000414592600006
dc.language.isoeng
dc.publisherCambridge Univ Press
dc.relation.ispartofJournal Of Developmental Origins Of Health And Disease
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectEndothelial dysfunctionen
dc.subjectEndothelial progenitor cellsen
dc.subjectIntrauterine growth restrictionen
dc.subjectNitric oxideen
dc.titleIntrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial functionen
dc.typeinfo:eu-repo/semantics/article
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