ArticlePloS one2016
Role of Nitric Oxide Isoforms in Vascular and Alveolar Development and Lung Injury in Vascular Endothelial Growth Factor Overexpressing Neonatal Mice Lungs.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Hyperoxia and pulmonary vascular injury in bronchopulmonary dysplasia: pathogenic mechanisms and emerging therapies-a systematic review.Pediatric research · 2026Pooled it
- Attenuation of Experimental Bronchopulmonary Dysplasia by Dimethyl Fumarate.Pediatric research · 2026Article
- Predictive value of increased C-reactive protein levels in preterm infants on respiratory function at five to six years of age.Communications medicine · 2026Article
- Tumor Progression Locus 2 Protects against Acute Respiratory Distress Syndrome in Influenza A Virus-Infected Mice.Microbiology spectrum · 2022Article
- Postnatal Sepsis and Bronchopulmonary Dysplasia in Premature Infants: Mechanistic Insights into "New BPD".American journal of respiratory cell and molecular biology · 2022Review
- Patho-mechanisms of the origins of bronchopulmonary dysplasia.Molecular and cellular pediatrics · 2021Review
- α1,3-Fucosyltransferase-IX, an enzyme of pulmonary endogenous lung stem cell marker SSEA-1, alleviates experimental bronchopulmonary dysplasia.Pediatric research · 2021Article
- Chitin Analog AVR-25 Prevents Experimental Bronchopulmonary Dysplasia.Journal of pediatric intensive care · 2020Article
- Signaling Pathways Involved in the Development of Bronchopulmonary Dysplasia and Pulmonary Hypertension.Children (Basel, Switzerland) · 2020Review
- Epigallocatechin-3-Gallate (EGCG), an Active Compound of Green Tea Attenuates Acute Lung Injury Regulating Macrophage Polarization and Krüpple-Like-Factor 4 (KLF4) Expression.Molecules (Basel, Switzerland) · 2020Article
- Genetic Strain and Sex Differences in a Hyperoxia-Induced Mouse Model of Varying Severity of Bronchopulmonary Dysplasia.The American journal of pathology · 2019Article
- Signaling interplay between primary cilia and nitric oxide: A mini review.Nitric oxide : biology and chemistry · 2018Review
- Early gestational mesenchymal stem cell secretome attenuates experimental bronchopulmonary dysplasia in part via exosome-associated factor TSG-6.Stem cell research & therapy · 2018Article
- The BPD trio? Interaction of dysregulated PDGF, VEGF, and TGF signaling in neonatal chronic lung disease.Molecular and cellular pediatrics · 2017Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
backgroundThe role of vascular endothelial growth factor (VEGF)-induced 3 different nitric oxide synthase (NOS) isoforms in lung development and injury in the newborn (NB) lung are not known. We hypothesized that VEGF-induced specific NOS pathways are critical regulators of lung development and injury. METHODOLOGY: We studied NB wild type (WT), lung epithelial cell-targeted VEGF165 doxycycline-inducible overexpressing transgenic (VEGFTG), VEGFTG treated with a NOS1 inhibitor (L-NIO), VEGFTG x NOS2-/- and VEGFTG x NOS3+/- mice in room air (RA) for 7 postnatal (PN) days. Lung morphometry (chord length), vascular markers (Ang1, Ang2, Notch2, vWF, CD31 and VE-cadherin), cell proliferation (Ki67), vascular permeability, injury and oxidative stress markers (hemosiderin, nitrotyrosine and 8-OHdG) were evaluated.
resultsVEGF overexpression in RA led to increased chord length and vascular markers at PN7, which were significantly decreased to control values in VEGFTG x NOS2-/- and VEGFTG x NOS3+/- lungs. However, we found no noticeable effect on chord length and vascular markers in the VEGFTG / NOS1 inhibited group. In the NB VEGFTG mouse model, we found VEGF-induced vascular permeability in the NB murine lung was partially dependent on NOS2 and NOS3-signaling pathways. In addition, the inhibition of NOS2 and NOS3 resulted in a significant decrease in VEGF-induced hemosiderin, nitrotyrosine- and 8-OHdG positive cells at PN7. NOS1 inhibition had no significant effect.
conclusionOur data showed that the complete absence of NOS2 and partial deficiency of NOS3 confers protection against VEGF-induced pathologic lung vascular and alveolar developmental changes, as well as injury markers. Inhibition of NOS1 does not have any modulating role on VEGF-induced changes in the NB lung. Overall, our data suggests that there is a significant differential regulation in the NOS-mediated effects of VEGF overexpression in the developing mouse lung.
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