ArticlePloS one2014
Remodeling of aorta extracellular matrix as a result of transient high oxygen exposure in newborn rats: implication for arterial rigidity and hypertension risk.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Role of Exercise in Visceral Adipose Tissue Inflammation and Macrophage Polarization in Hypertensive Mice.International journal of molecular sciences · 2025Article
- Increased uterine arterial tone, stiffness and remodeling with augmented matrix metalloproteinase-1 and -7 in uteroplacental ischemia-induced hypertensive pregnancy.Biochemical pharmacology · 2024Article
- Retinal microvascular complexity as a putative biomarker of biological age: a pilot study.Biogerontology · 2023Article
- Increased CaBiochemical pharmacology · 2023Article
- Educational Review: The Impact of Perinatal Oxidative Stress on the Developing Kidney.Frontiers in pediatrics · 2022Review
- Apelin expression deficiency in mice contributes to vascular stiffening by extracellular matrix remodeling of the aortic wall.Scientific reports · 2021Article
- Impact of the Vulnerable Preterm Heart and Circulation on Adult Cardiovascular Disease Risk.Hypertension (Dallas, Tex. : 1979) · 2020Review
- Increased aortic stiffness and elevated blood pressure in response to exercise in adult survivors of prematurity.Physiological reports · 2020Article
- Neonatal hyperoxia exposure induces aortic biomechanical alterations and cardiac dysfunction in juvenile rats.Physiological reports · 2020Article
- Endothelial colony-forming cell therapy for heart morphological changes after neonatal high oxygen exposure in rats, a model of complications of prematurity.Physiological reports · 2018Article
- Neonatal hyperoxia depletes pulmonary vein cardiomyocytes in adult mice via mitochondrial oxidation.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Preterm Birth and Hypertension: Is There a Link?Current hypertension reports · 2016Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Neonatal high-oxygen exposure leads to elevated blood pressure, microvascular rarefaction, vascular dysfunction and arterial (aorta) rigidity in adult rats. Whether structural changes are present in the matrix of aorta wall is unknown. Considering that elastin synthesis peaks in late fetal life in humans, and early postnatal life in rodents, we postulated that transient neonatal high-oxygen exposure can trigger premature vascular remodelling. Sprague Dawley rat pups were exposed from days 3 to 10 after birth to 80% oxygen (vs. room air control) and were studied at 4 weeks. Blood pressure and vasomotor response of the aorta to angiotensin II and to the acetylcholine analogue carbachol were not different between groups. Vascular superoxide anion production was similar between groups. There was no difference between groups in aortic cross sectional area, smooth muscle cell number or media/lumen ratio. In oxygen-exposed rats, aorta elastin/collagen content ratio was significantly decreased, the expression of elastinolytic cathepsin S was increased whereas collagenolytic cathepsin K was decreased. By immunofluorescence we observed an increase in MMP-2 and TIMP-1 staining in aortas of oxygen-exposed rats whereas TIMP-2 staining was reduced, indicating a shift in the balance towards degradation of the extra-cellular matrix and increased deposition of collagen. There was no significant difference in MMP-2 activity between groups as determined by gelatin zymography. Overall, these findings indicate that transient neonatal high oxygen exposure leads to vascular wall alterations (decreased elastin/collagen ratio and a shift in the balance towards increased deposition of collagen) which are associated with increased rigidity. Importantly, these changes are present prior to the elevation of blood pressure and vascular dysfunction in this model, and may therefore be contributory.
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