Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development. - Wikidata - wikimedia - TriplyDB

Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development.

Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development.

http://www.wikidata.org/entity/Q50721829

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Consequences of hyperoxia and the toxicity of oxygen in the lung Affect of Early Life Oxygen Exposure on Proper Lung Development and Response to Respiratory Viral Infections Neonatal oxygen increases sensitivity to influenza A virus infection in adult mice by suppressing epithelial expression of Ear1 Adenosine A2B receptors are highly expressed on murine type II alveolar epithelial cells.Expression level and subcellular localization of heme oxygenase-1 modulates its cytoprotective properties in response to lung injury: a mouse model Neonatal hyperoxia stimulates the expansion of alveolar epithelial type II cells Epithelial repair mechanisms in the lung Thioredoxin-1 redox signaling regulates cell survival in response to hyperoxia.Heme oxygenase in neonatal lung injury and repair Maternal docosahexaenoic acid supplementation decreases lung inflammation in hyperoxia-exposed newborn mice.Neonatal hyperoxia leads to persistent alterations in NK responses to influenza A virus infection.Effect of recombinant IL-10 on cultured fetal rat alveolar type II cells exposed to 65%-hyperoxia.Neonatal hyperoxia causes pulmonary vascular disease and shortens life span in aging mice Alteration in the Wnt microenvironment directly regulates molecular events leading to pulmonary senescence Cumulative neonatal oxygen exposure predicts response of adult mice infected with influenza A virus.Silencing hyperoxia-induced C/EBPα in neonatal mice improves lung architecture via enhanced proliferation of alveolar epithelial cells Cigarette-Smoke-Induced Dysregulation of MicroRNA Expression and Its Role in Lung Carcinogenesis.Aberrant signaling pathways of the lung mesenchyme and their contributions to the pathogenesis of bronchopulmonary dysplasia Aryl hydrocarbon receptor is necessary to protect fetal human pulmonary microvascular endothelial cells against hyperoxic injury: Mechanistic roles of antioxidant enzymes and RelB Early exposure to hyperoxia or hypoxia adversely impacts cardiopulmonary development rIL-10 enhances IL-10 signalling proteins in foetal alveolar type II cells exposed to hyperoxia Enolase 1 (ENO1) and protein disulfide-isomerase associated 3 (PDIA3) regulate Wnt/β-catenin-driven trans-differentiation of murine alveolar epithelial cells.Hyperoxia enhances VEGF release from A549 cells via post-transcriptional processes.Lung development and the host response to influenza A virus are altered by different doses of neonatal oxygen in mice.Inhaled ethyl nitrite prevents hyperoxia-impaired postnatal alveolar development in newborn rats.Adrenomedullin deficiency potentiates hyperoxic injury in fetal human pulmonary microvascular endothelial cells.Memory CD8+ T cells are sufficient to alleviate impaired host resistance to influenza A virus infection caused by neonatal oxygen supplementation.Detoxification of Mitochondrial Oxidants and Apoptotic Signaling Are Facilitated by Thioredoxin-2 and Peroxiredoxin-3 during Hyperoxic Injury.Expression of SP-C and Ki67 in lungs of preterm infants dying from respiratory distress syndrome Omeprazole does not Potentiate Acute Oxygen Toxicity in Fetal Human Pulmonary Microvascular Endothelial Cells Exposed to Hyperoxia.Evaluation of Radiation-induced Class V Dental Caries in Patients with Head and Neck Cancers Undergoing Radiotherapy.Interleukin-10 down-regulates cathepsin B expression in fetal rat alveolar type II cells exposed to hyperoxia.Neonatal hyperoxia enhances the inflammatory response in adult mice infected with influenza A virus.Neonatal hyperoxia increases sensitivity of adult mice to bleomycin-induced lung fibrosis.Wnt3a Mediates the Inhibitory Effect of Hyperoxia on the Transdifferentiation of AECIIs to AECIs.The Oxygen Environment at Birth Specifies the Population of Alveolar Epithelial Stem Cells in the Adult Lung.Developmental differences in hyperoxia-induced oxidative stress and cellular responses in the murine lung.Lung alveolar integrity is compromised by telomere shortening in telomerase-null mice.Hyperoxia-induced NF-kappaB activation occurs via a maturationally sensitive atypical pathway Nrf2 increases survival and attenuates alveolar growth inhibition in neonatal mice exposed to hyperoxia

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Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development.

http://www.wikidata.org/entity/Q50721829

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Type II epithelial cells are c ...... of postnatal lung development.

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Jason M Roper

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Michael A O'Reilly

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Rhonda J Staversky

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Sharon A McGrath-Morrow

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Terry W Wright

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William M Maniscalco

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P2860

Loss of HIF-2alpha and inhibition of VEGF impair fetal lung maturation, whereas treatment with VEGF prevents fatal respiratory distress in premature mice

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

Normal remodeling of the oxygen-injured lung requires the cyclin-dependent kinase inhibitor p21(Cip1/WAF1/Sdi1)

Vascular endothelial growth factor co-ordinates proper development of lung epithelium and vasculature

Hyperoxia-induced apoptosis and Fas/FasL expression in lung epithelial cells.

Long term sequelae of bronchopulmonary dysplasia (chronic lung disease of infancy).

Alveolar type I cells: molecular phenotype and development.

Lung function eight years after neonatal ventilation.

Control mechanisms of lung alveolar development and their disorders in bronchopulmonary dysplasia.

Apoptosis in neonatal murine lung exposed to hyperoxia.

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