ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Antenatal glucocorticoids counteract LPS changes in TGF-β pathway and caveolin-1 in ovine fetal lung.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. 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, 34 citations in OpenAlex.
- Fetal origin of bronchopulmonary dysplasia: contribution of intrauterine inflammation.Molecular medicine (Cambridge, Mass.) · 2024Review
- Development of a blood proteins-based model for bronchopulmonary dysplasia prediction in premature infants.BMC pediatrics · 2023Article
- Complex roles of TGF-β signaling pathways in lung development and bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Acute Lung Functional and Airway Remodeling Effects of an Inhaled Highly Selective Phosphodiesterase 4 Inhibitor in Ventilated Preterm Lambs Exposed to Chorioamnionitis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- When inflammation meets lung development-an update on the pathogenesis of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2022Review
- A20 Is Increased in Fetal Lung in a Sheep LPS Model of Chorioamnionitis.Oxidative medicine and cellular longevity · 2022Article
- Early origins of lung disease: towards an interdisciplinary approach.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Signaling Pathways Involved in the Development of Bronchopulmonary Dysplasia and Pulmonary Hypertension.Children (Basel, Switzerland) · 2020Review
- Caffeine modulates glucocorticoid-induced expression of CTGF in lung epithelial cells and fibroblasts.Respiratory research · 2017Article
- Looking ahead: where to next for animal models of bronchopulmonary dysplasia?Cell and tissue research · 2017Review
- The Future of Bronchopulmonary Dysplasia: Emerging Pathophysiological Concepts and Potential New Avenues of Treatment.Frontiers in medicine · 2017Review
- Can the preterm lung recover from perinatal stress?Molecular and cellular pediatrics · 2016Review
- Can maternal DHA supplementation offer long-term protection against neonatal hyperoxic lung injury?American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Respiratory consequences of prematurity: evolution of a diagnosis and development of a comprehensive approach.Journal of perinatology : official journal of the California Perinatal Association · 2015Review
- Protective Effects of Valproic Acid, a Histone Deacetylase Inhibitor, against Hyperoxic Lung Injury in a Neonatal Rat Model.PloS one · 2015Article
- Glucocorticoids recruit Tgfbr3 and Smad1 to shift transforming growth factor-β signaling from the Tgfbr1/Smad2/3 axis to the Acvrl1/Smad1 axis in lung fibroblasts.The Journal of biological chemistry · 2014Article
- Deregulation of the lysyl hydroxylase matrix cross-linking system in experimental and clinical bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Caffeine and rolipram affect Smad signalling and TGF-β1 stimulated CTGF and transgelin expression in lung epithelial cells.PloS one · 2014Article
- Perinatal factors in neonatal and pediatric lung diseases.Expert review of respiratory medicine · 2013Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Inflammation and antenatal glucocorticoids, the latter given to mothers at risk for preterm birth, affect lung development and may contribute to the development of bronchopulmonary dysplasia (BPD). The effects of the combined exposures on inflammation and antenatal glucocorticoids on transforming growth factor (TGF)-β signaling are unknown. TGF-β and its downstream mediators are implicated in the etiology of BPD. Therefore, we asked whether glucocorticoids altered intra-amniotic lipopolysaccharide (LPS) effects on TGF-β expression, its signaling molecule phosphorylated sma and mothers against decapentaplegic homolog 2 (pSmad2), and the downstream mediators connective tissue growth factor (CTGF) and caveolin-1 (Cav-1). Ovine singleton fetuses were randomized to receive either an intra-amniotic injection of LPS and/or maternal betamethasone (BTM) intramuscularly 7 and/or 14 days before delivery at 120 days gestational age (GA; term = 150 days GA). Saline was used for controls. Protein levels of TGF-β1 and -β2 were measured by ELISA. Smad2 phosphorylation was assessed by immunohistochemistry and Western blot. CTGF and Cav-1 mRNA and protein levels were determined by RT-PCR and Western blot. Free TGF-β1 and -β2 and total TGF-β1 levels were unchanged after LPS and/or BTM exposure, although total TGF-β2 increased in animals exposed to BTM 7 days before LPS. pSmad2 immunostaining increased 7 days after LPS exposure although pSmad2 protein expression did not increase. Similarly, CTGF mRNA and protein levels increased 7 days after LPS exposure as Cav-1 mRNA and protein levels decreased. BTM exposure before LPS prevented CTGF induction and Cav-1 downregulation. This study demonstrated that the intrauterine inflammation-induced TGF-β signaling can be inhibited by antenatal glucocorticoids in fetal lungs.
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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.