Intrauterine growth restriction-induced deleterious adaptations in endothelial progenitor cells: possible mechanism to impair endothelial function
| Autor: | M. H. C. de Carvalho, V. Oliveira, Eliana Hiromi Akamine, Lisete Compagno Michelini, Tiago Fernandes, E. de Oliveira, Maria do Carmo Franco, L. V. de Souza, Silva Junior |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine Senescence medicine.medical_specialty Medicine (miscellaneous) Intrauterine growth restriction Vasodilation 030204 cardiovascular system & hematology Nitric Oxide medicine.disease_cause Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Pregnancy Enos Internal medicine medicine Animals Rats Wistar Progenitor cell Endothelial dysfunction Endothelial Progenitor Cells Fetal Growth Retardation biology business.industry medicine.disease biology.organism_classification Rats Oxidative Stress 030104 developmental biology Endocrinology chemistry embryonic structures cardiovascular system Female Endothelium Vascular business Oxidative stress |
| Zdroj: | Journal of Developmental Origins of Health and Disease. 8:665-673 |
| ISSN: | 2040-1752 2040-1744 |
| DOI: | 10.1017/s2040174417000484 |
| Popis: | 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 anad libitumdiet (control group) or 50% of thead libitumdiet (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 assessedin 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 senescencein vitro. These findings may contribute towards elucidating the possible mechanisms involved in endothelial dysfunction induced by fetal programming. |
| Databáze: | OpenAIRE |
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