Moderate hyperoxia induces senescence in developing human lung fibroblasts

Hyperoxia exposure in premature infants increases the risk of subsequent lung diseases, such as asthma and bronchopulmonary dysplasia. Fibroblasts help maintain bronchial and alveolar integrity. Thus, understanding mechanisms by which hyperoxia influences fibroblasts is critical. Cellular senescence...

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Veröffentlicht in:	American journal of physiology. Lung cellular and molecular physiology 2019-11, Vol.317 (5), p.L525-L536
Hauptverfasser:	You, Kai, Parikh, Pavan, Khandalavala, Karl, Wicher, Sarah A, Manlove, Logan, Yang, Binxia, Roesler, Annie, Roos, Ben B, Teske, Jacob J, Britt, Jr, Rodney D, Pabelick, Christina M, Prakash, Y S
Format:	Artikel
Sprache:	eng
Schlagworte:	Alveoli Asthma Autophagy Autophagy - drug effects Autophagy - genetics Biomarkers CCAAT-Enhancer-Binding Protein-beta - genetics CCAAT-Enhancer-Binding Protein-beta - metabolism Cell cycle Cell Proliferation - drug effects Cell size Cellular Senescence - drug effects Cellular Senescence - genetics Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism Damage assessment Deoxyribonucleic acid DNA DNA Damage Dysplasia Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects Etoposide Etoposide - pharmacology Extracellular matrix Extracellular Matrix - chemistry Extracellular Matrix - drug effects Extracellular Matrix - metabolism Fetus Fetuses Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism G2 Phase Cell Cycle Checkpoints - drug effects G2 Phase Cell Cycle Checkpoints - genetics Galactosidase Gene expression Gene Expression Regulation - drug effects Humans Hyperoxia Hyperoxia - genetics Hyperoxia - metabolism Infants Inflammation Interleukin 1 Interleukin 6 Interleukin 8 Interleukin-1 - genetics Interleukin-1 - metabolism Interleukin-8 - genetics Interleukin-8 - metabolism Lung - cytology Lung - metabolism Lung diseases Matrix Metalloproteinase 3 - genetics Matrix Metalloproteinase 3 - metabolism Oxygen - pharmacology p53 Protein Phagocytosis Phenotypes Plasminogen Activator Inhibitor 1 - genetics Plasminogen Activator Inhibitor 1 - metabolism Primary Cell Culture Secretome Senescence Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism β-Galactosidase
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Beschreibung
Zusammenfassung:	Hyperoxia exposure in premature infants increases the risk of subsequent lung diseases, such as asthma and bronchopulmonary dysplasia. Fibroblasts help maintain bronchial and alveolar integrity. Thus, understanding mechanisms by which hyperoxia influences fibroblasts is critical. Cellular senescence is increasingly recognized as important to the pathophysiology of multiple diseases. We hypothesized that clinically relevant moderate hyperoxia (
ISSN:	1040-0605 1522-1504
DOI:	10.1152/ajplung.00067.2019