ArticleReproductive sciences (Thousand Oaks, Calif.)2011
Antenatal maternal hypoxic stress: adaptations in fetal lung Renin-Angiotensin system.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- Epigenetic Regulation of the Renin-Angiotensin-Aldosterone System in Hypertension.International journal of molecular sciences · 2024Review
- Elevated Vascular Sympathetic Neurotransmission and Remodelling Is a Common Feature in a Rat Model of Foetal Programming of Hypertension and SHR.Biomedicines · 2022Article
- Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling.International journal of molecular sciences · 2022Article
- Programming of Vascular Dysfunction by Maternal Stress: Immune System Implications.Frontiers in physiology · 2022Review
- Role of the Uteroplacental Renin-Angiotensin System in Placental Development and Function, and Its Implication in the Preeclampsia Pathogenesis.Biomedicines · 2021Review
- Effects of SARS-COV-2 infection on fetal pulmonary artery Doppler parameters.Echocardiography (Mount Kisco, N.Y.) · 2021Article
- Fetal Growth Restriction and Hypertension in the Offspring: Mechanistic Links and Therapeutic Directions.The Journal of pediatrics · 2020Review
- Fetal brain sparing in a mouse model of chronic maternal hypoxia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Fetal Cerebrovascular Maturation: Effects of Hypoxia.Seminars in pediatric neurology · 2018Review
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Liraglutide Enhances the Activity of the ACE-2/Ang(1-7)/Mas Receptor Pathway in Lungs of Male Pups from Food-Restricted Mothers and Prevents the Reduction of SP-A.International journal of endocrinology · 2018Article
- Developmental acceleration of bradykinin-dependent relaxation by prenatal chronic hypoxia impedes normal development after birth.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Antenatal maternal low protein diet: ACE-2 in the mouse lung and sexually dimorphic programming of hypertension.BMC physiology · 2015Article
- Antenatal maternal hypoxia: criterion for fetal growth restriction in rodents.Frontiers in physiology · 2015Review
- MicroRNAs: potential regulators of renal development genes that contribute to CAKUT.Pediatric nephrology (Berlin, Germany) · 2014Review
- Maternal protein restriction alters VEGF signaling and decreases pulmonary alveolar in fetal rats.International journal of clinical and experimental pathology · 2014Article
- Maternal stress induces epigenetic signatures of psychiatric and neurological diseases in the offspring.PloS one · 2013Article
- Local fetal lung renin-angiotensin system as a target to treat congenital diaphragmatic hernia.Molecular medicine (Cambridge, Mass.) · 2012Article
- Antenatal maternal hypoxic stress: adaptations of the placental renin-angiotensin system in the mouse.Placenta · 2011Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Antenatal maternal hypoxia (AMH) can lead to intrauterine growth restriction (IUGR), as well as idiopathic pulmonary hypertension of newborn and adult, the latter of which may be a consequence of alterations in the local pulmonary renin-angiotensin system (RAS). Little is known of these adaptations, however. Thus, we tested the hypothesis that antenatal maternal hypoxia is associated with alterations in gene and protein expression of the pulmonary renin-angiotensin system, which may play an important role in pulmonary disorders in the offspring. In FVB/NJ mice, we studied messenger RNA (mRNA) and protein expression, as well as promoter DNA methylation and microRNA (miRNA) levels in response to 48 hours hypoxia (10.5% O(2)) at 15.5 day post coitum (DPC). In response to AMH, the pulmonary mRNA levels of angiotensin-converting enzyme (ACE) 1.2, ACE-2, and angiotensin II type 1b (AT-1b) receptors were increased significantly, as compared to controls (N = 4). In response to antenatal hypoxia, pulmonary protein levels of renin and ACE-2 also were increased significantly, whereas ACE-1 protein expression was reduced. In fetal lungs, we also observed reduced expression of the miRNAs: mmu-mir -199b, -27b, -200b, and -468 that putatively increase the translation of renin, ACE-1, ACE-2, and AT-1 receptors, respectively. In response to AMH, promoter methylation of ACE was unchanged. We conclude that AMH leads to changes in expression of pulmonary RAS of fetal mice. The possible implications of these changes for the regulation of pulmonary vascular contractility in later life remain to be explored.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.