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

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

Author Oliveira, V. Autor UNIFESP Google Scholar
de Souza, L. V. Autor UNIFESP Google Scholar
Fernandes, T. Google Scholar
Junior, S. D. S. Google Scholar
de Carvalho, M. H. C. Google Scholar
Akamine, E. H. Google Scholar
Michelini, L. C. Google Scholar
de Oliveira, E. M. Google Scholar
Franco, M. D. C. Autor UNIFESP Google Scholar
Abstract Intrauterine 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.
Keywords endothelial dysfunction
endothelial progenitor cells
intrauterine growth restriction
nitric oxide
xmlui.dri2xhtml.METS-1.0.item-coverage Cambridge
Language English
Sponsor FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo, Brazil)
Grant number FAPESP: 2013/03139-0
FAPESP: 2013/00311-6
Date 2017
Published in Journal Of Developmental Origins Of Health And Disease. Cambridge, v. 8, n. 6, p. 665-673, 2017.
ISSN 2040-1744 (Sherpa/Romeo, impact factor)
Publisher Cambridge Univ Press
Extent 665-673
Origin http://dx.doi.org/10.1017/S2040174417000484
Access rights Closed access
Type Article
Web of Science ID WOS:000414592600006
URI https://repositorio.unifesp.br/handle/11600/58151

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