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

Autor(es)

Oliveira, V. ^[1] ; de Souza, L. V. ^[1] ; Fernandes, T. ^[2] ; Junior, S. D. S. ^[3] ; de Carvalho, M. H. C. ^[4] ; Akamine, E. H. ^[4] ; Michelini, L. C. ^[3] ; de Oliveira, E. M. ^[2] ; Franco, M. D. C. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Fed Sao Paulo, Sch Med, Nephrol Div, Rua Botucatu 703, BR-04023062 Sao Paulo, SP - Brazil

^[2] Univ Sao Paulo, Sch Phys Educ & Sport, Biochem & Mol Biol Lab, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci, Physiol Dept, Sao Paulo - Brazil

^[4] Univ Sao Paulo, Inst Biomed Sci, Pharmacol Dept, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE; v. 8, n. 6, p. 665-673, DEC 2017.
• Citações Web of Science: 2

Resumo

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. (AU)

• Processo FAPESP: 13/00311-6 - Isolamento e caracterização de células progenitoras endoteliais circulantes e de medula óssea de ratos submetidos à restrição de nutrientes in útero: avaliação do impacto do treinamento físico aeróbio e do balanço redox
• Beneficiário: Vanessa Aparecida de Oliveira
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 13/03139-0 - Inter-relação do peso ao nascer, treinamento físico e níveis pressóricos: uma abordagem clínica e experimental sobre o papel das células progenitoras endoteliais
• Beneficiário: Maria Do Carmo Pinho Franco
• Modalidade de apoio: Auxílio à Pesquisa - Regular