ArticlePediatric research2009
Chronic in utero cyclooxygenase inhibition alters PGE2-regulated ductus arteriosus contractile pathways and prevents postnatal closure.
Article in Pediatric research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03022253 (Liberal Versus Restrictive Platelet Transfusion for Treatment of Hemodynamically Significant Patent Ductus Arteriosus in Thrombocytopenic Preterm Neonates- A Randomized Open Label, Controlled Trial), which is not on this map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Liberal Versus Restrictive Platelet Transfusion for Treatment of Hemodynamically Significant Patent Ductus Arteriosus in Thrombocytopenic Preterm Neonates- A Randomized Open Label, Controlled Trial
Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- A novel role for PGEAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Mouse models of patent ductus arteriosus (PDA) and their relevance for human PDA.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Review
- Role of Tissue-Type Plasminogen Activator in Remodeling of the Ductus Arteriosus.Circulation reports · 2020Review
- Understanding the pathobiology in patent ductus arteriosus in prematurity-beyond prostaglandins and oxygen.Pediatric research · 2019Review
- Effects of antenatal betamethasone on preterm human and mouse ductus arteriosus: comparison with baboon data.Pediatric research · 2018Article
- Novel drug targets for ductus arteriosus manipulation: Looking beyond prostaglandins.Seminars in perinatology · 2018Review
- Effects of Advancing Gestation and Non-Caucasian Race on Ductus Arteriosus Gene Expression.The Journal of pediatrics · 2015Article
- Characterization of transcription factor AP-2 β mutations involved in familial isolated patent ductus arteriosus suggests haploinsufficiency.The Journal of surgical research · 2014Article
- Association of amino acids with common complications of prematurity.Pediatric research · 2013Article
- Omental grafting: a cell-based therapy for blood vessel repair.Journal of tissue engineering and regenerative medicine · 2013Article
- Current Perspectives on Pathobiology of the Ductus Arteriosus.Journal of clinical & experimental cardiology · 2012Article
- Patterns of gene expression in the ductus arteriosus are related to environmental and genetic risk factors for persistent ductus patency.Pediatric research · 2010Article
- Inadvertent relaxation of the ductus arteriosus by pharmacologic agents that are commonly used in the neonatal period.Seminars in perinatology · 2010Review
- Failure of postnatal ductus arteriosus closure in prostaglandin transporter-deficient mice.Circulation · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Although prostaglandin E2 (PGE2) vasodilates the ductus arteriosus, tocolysis with cyclooxygenase (COX) inhibitors delays postnatal ductus arteriosus closure. We used fetal mice and sheep to determine whether PGE2 has a role in the development of ductus contractility that is distinct from its function as a vasodilator. Prolonged exposure of fetal ductus to PGE2 in vitro increased the expression of CaL- and K+-channel genes (CaLalpha1c, CaLbeta2, Kir6.1, and Kv1.5, which regulate oxygen-induced constriction) without affecting the genes that regulate Rho-kinase-mediated calcium sensitization. Conversely, chronic exposure to COX inhibitors in utero decreased expression of CaL- and K+-channel genes, without affecting Rho-kinase-associated genes. Chronic COX inhibition in utero decreased the ductus' in vitro contractile response to stimuli that use CaL- and K+-channels (like O2 and K+), whereas the response to stimuli that act through Rho-kinase-mediated pathways (like U46619) was not significantly affected. Phosphodiesterase expression, which decreases the ductus' sensitivity to cAMP- or cGMP-dependent vasodilators, was increased by PGE2 exposure and decreased by COX inhibition, respectively. These studies identify potential downstream effectors of a PGE2-mediated, developmental program, regulating oxygen-induced ductus closure. Alterations in these effectors may explain the increased risk of patent ductus arteriosus (PDA) after in utero COX inhibition.
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Registered trials
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.