Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood

Abstract Adverse perinatal conditions can lead to developmental programming of cardiovascular diseases. Prematurely born infants are often exposed to high oxygen levels, which in animal models has been associated with endothelial dysfunction, hypertension, and cardiac remodeling during adulthood. He...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Raphael Mathieu, Sylvie Dussault, Michel Desjarlais, François Rivard, Wahiba Dhahri, Anik Cloutier, Anne-Monique Nuyt, Alain Rivard
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
Materias:
R
Q
Acceso en línea:https://doaj.org/article/f82ba77dde434355ab36b34a1d84dc4e
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:f82ba77dde434355ab36b34a1d84dc4e
record_format dspace
spelling oai:doaj.org-article:f82ba77dde434355ab36b34a1d84dc4e2021-12-02T11:52:44ZNeonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood10.1038/s41598-017-14396-82045-2322https://doaj.org/article/f82ba77dde434355ab36b34a1d84dc4e2017-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-14396-8https://doaj.org/toc/2045-2322Abstract Adverse perinatal conditions can lead to developmental programming of cardiovascular diseases. Prematurely born infants are often exposed to high oxygen levels, which in animal models has been associated with endothelial dysfunction, hypertension, and cardiac remodeling during adulthood. Here we found that adult mice that have been transiently exposed to O2 after birth show defective neovasculariation after hindlimb ischemia, as demonstrated by impaired blood flow recovery, reduced vascular density in ischemic muscles and increased tissue damages. Ischemic muscles isolated from mice exposed to O2 after birth exhibit increased oxidative stress levels and reduced expression of superoxide dismutase 1 (SOD1) and vascular endothelial growth factor (VEGF). Pro-angiogenic cells (PACs) have been shown to have an important role for postnatal neovascularisation. We found that neonatal exposure to O2 is associated with reduced number of PACs in adults. Moreover, the angiogenic activities of both PACs and mature mouse aortic endothelial cells (MAECs) are significantly impaired in mice exposed to hyperoxia after birth. Our results indicate that neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization during adulthood. The mechanism involves deleterious effects on oxidative stress levels and angiogenic signals in ischemic muscles, together with dysfunctional activities of PACs and mature endothelial cells.Raphael MathieuSylvie DussaultMichel DesjarlaisFrançois RivardWahiba DhahriAnik CloutierAnne-Monique NuytAlain RivardNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Raphael Mathieu
Sylvie Dussault
Michel Desjarlais
François Rivard
Wahiba Dhahri
Anik Cloutier
Anne-Monique Nuyt
Alain Rivard
Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
description Abstract Adverse perinatal conditions can lead to developmental programming of cardiovascular diseases. Prematurely born infants are often exposed to high oxygen levels, which in animal models has been associated with endothelial dysfunction, hypertension, and cardiac remodeling during adulthood. Here we found that adult mice that have been transiently exposed to O2 after birth show defective neovasculariation after hindlimb ischemia, as demonstrated by impaired blood flow recovery, reduced vascular density in ischemic muscles and increased tissue damages. Ischemic muscles isolated from mice exposed to O2 after birth exhibit increased oxidative stress levels and reduced expression of superoxide dismutase 1 (SOD1) and vascular endothelial growth factor (VEGF). Pro-angiogenic cells (PACs) have been shown to have an important role for postnatal neovascularisation. We found that neonatal exposure to O2 is associated with reduced number of PACs in adults. Moreover, the angiogenic activities of both PACs and mature mouse aortic endothelial cells (MAECs) are significantly impaired in mice exposed to hyperoxia after birth. Our results indicate that neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization during adulthood. The mechanism involves deleterious effects on oxidative stress levels and angiogenic signals in ischemic muscles, together with dysfunctional activities of PACs and mature endothelial cells.
format article
author Raphael Mathieu
Sylvie Dussault
Michel Desjarlais
François Rivard
Wahiba Dhahri
Anik Cloutier
Anne-Monique Nuyt
Alain Rivard
author_facet Raphael Mathieu
Sylvie Dussault
Michel Desjarlais
François Rivard
Wahiba Dhahri
Anik Cloutier
Anne-Monique Nuyt
Alain Rivard
author_sort Raphael Mathieu
title Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
title_short Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
title_full Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
title_fullStr Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
title_full_unstemmed Neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
title_sort neonatal exposure to high oxygen levels leads to impaired ischemia-induced neovascularization in adulthood
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/f82ba77dde434355ab36b34a1d84dc4e
work_keys_str_mv AT raphaelmathieu neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT sylviedussault neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT micheldesjarlais neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT francoisrivard neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT wahibadhahri neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT anikcloutier neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT annemoniquenuyt neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
AT alainrivard neonatalexposuretohighoxygenlevelsleadstoimpairedischemiainducedneovascularizationinadulthood
_version_ 1718394962494619648