Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia - Wikidata - wikimedia - TriplyDB

Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia

Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia

http://www.wikidata.org/entity/Q37140927

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Consequences of hyperoxia and the toxicity of oxygen in the lung Superoxide dismutase 3, extracellular (SOD3) variants and lung function The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source Affect of Early Life Oxygen Exposure on Proper Lung Development and Response to Respiratory Viral Infections Maternal diesel inhalation increases airway hyperreactivity in ozone-exposed offspring Increased expression of catalase and superoxide dismutase 2 reduces cone cell death in retinitis pigmentosa.Oxygen, gastrin-releasing Peptide, and pediatric lung disease: life in the balance.Disrupted postnatal lung development in heme oxygenase-1 deficient mice.Superoxide dismutase 3 dysregulation in a murine model of neonatal lung injury The role of genetic polymorphisms in antioxidant enzymes and potential antioxidant therapies in neonatal lung disease Developmental regulation of antioxidant enzymes and their impact on neonatal lung disease Elastase inhibitory activity of airway α1-antitrypsin is protected by treatment with a catalytic antioxidant in a baboon model of severe bronchopulmonary dysplasia.Mechanisms of dysfunction in senescent pulmonary endothelium.Superoxide dismutase 3 limits collagen-induced arthritis in the absence of phagocyte oxidative burst Inhaled ethyl nitrite prevents hyperoxia-impaired postnatal alveolar development in newborn rats.NADPH oxidase-derived ROS and the regulation of pulmonary vessel tone Superoxide dismutase 3 controls adaptive immune responses and contributes to the inhibition of ovalbumin-induced allergic airway inflammation in mice.Lack of EC-SOD worsens alveolar and vascular development in a neonatal mouse model of bleomycin-induced bronchopulmonary dysplasia and pulmonary hypertension.Metallothionein-induced zinc partitioning exacerbates hyperoxic acute lung injury.The role of hyperoxia in the pathogenesis of experimental BPD.Pulmonary alveolar epithelial uptake of S-nitrosothiols is regulated by L-type amino acid transporter.Lung EC-SOD overexpression attenuates hypoxic induction of Egr-1 and chronic hypoxic pulmonary vascular remodeling.The Oxygen Environment at Birth Specifies the Population of Alveolar Epithelial Stem Cells in the Adult Lung.Hyperoxia impairs postnatal alveolar epithelial development via NADPH oxidase in newborn mice Neonatal oxygen adversely affects lung function in adult mice without altering surfactant composition or activity.Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways.Acute lung injury and pulmonary vascular permeability: use of transgenic models.Antioxidant strategies and respiratory disease of the preterm newborn: an update Gene Expression Profile of NF-κB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid.SOD2 activity is not impacted by hyperoxia in murine neonatal pulmonary artery smooth muscle cells and mice.Interaction between oxidative stress sensor Nrf2 and xenobiotic-activated aryl hydrocarbon receptor in the regulation of the human phase II detoxifying UDP-glucuronosyltransferase 1A10.Sustained lung activity of a novel chimeric protein, SOD2/3, after intratracheal administration.Zinc(II) ion promotes anti-inflammatory effects of rhSOD3 by increasing cellular association.The R213G polymorphism in SOD3 protects against allergic airway inflammation.Gene transfer of extracellular superoxide dismutase ameliorates pulmonary hypertension in rats.Neonatal hyperoxia depletes pulmonary vein cardiomyocytes in adult mice via mitochondrial oxidation.Can We Understand the Pathobiology of Bronchopulmonary Dysplasia?Redistribution of Extracellular Superoxide Dismutase Causes Neonatal Pulmonary Vascular Remodeling and PH but Protects Against Experimental Bronchopulmonary Dysplasia.

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Transgenic extracellular superoxide dismutase protects postnatal alveolar epithelial proliferation and development during hyperoxia

http://www.wikidata.org/entity/Q37140927

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 12 August 2005

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Transgenic extracellular super ...... d development during hyperoxia

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Transgenic extracellular super ...... development during hyperoxia.

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Transgenic extracellular super ...... d development during hyperoxia

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Transgenic extracellular super ...... development during hyperoxia.

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Transgenic extracellular super ...... d development during hyperoxia

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Transgenic extracellular super ...... development during hyperoxia.

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AJPLUNG.00133.2005

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American Journal of Physiology - Lung Cellular and Molecular Physiology

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Transgenic extracellular super ...... d development during hyperoxia

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Eva Nozik-Grayck

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Mary H Whorton

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Michael A O'Reilly

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Richard L Auten

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Tim D Oury

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P2860

Brief 95% O2 exposure effects on surfactant protein and mRNA in rat alveolar and bronchiolar epithelium

Extracellular superoxide dismutase in biology and medicine

Identification of PA2.26 antigen as a novel cell-surface mucin-type glycoprotein that induces plasma membrane extensions and increased motility in keratinocytes

T1alpha/podoplanin deficiency disrupts normal lymphatic vasculature formation and causes lymphedema

T1alpha, a lung type I cell differentiation gene, is required for normal lung cell proliferation and alveolus formation at birth

Participation of p53 protein in the cellular response to DNA damage

Extracellular superoxide dismutase in the airways of transgenic mice reduces inflammation and attenuates lung toxicity following hyperoxia

DNA damage and cell cycle checkpoints in hyperoxic lung injury: braking to facilitate repair.

Lung epithelial stem cells.

Superoxide dismutases in the lung and human lung diseases.

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