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Melatonin Protects Against Hyperoxia-Induced Apoptosis in Alveolar Epithelial type II  Cells by Activating the MT2/PI3K/AKT/ETS1 Signaling Pathway
ConclusionMelatonin prevents hyperoxia-induced apoptosis by activating the MT2/PI3K/AKT/ETS1 axis in alveolar epithelial cells.
Source: Lung - March 17, 2023 Category: Respiratory Medicine Source Type: research

Sphingosine kinase 1 regulates lysyl oxidase through STAT3 in hyperoxia-mediated neonatal lung injury
Conclusion HO-induced SPHK1/S1P signalling axis plays a critical role in transcriptional regulation of LOX expression via SPNS2, S1P1 and STAT3 in lung endothelium.
Source: Thorax - December 16, 2021 Category: Respiratory Medicine Authors: Ha, A. W., Bai, T., Ebenezer, D. L., Sethi, T., Sudhadevi, T., Mangio, L. A., Garzon, S., Pryhuber, G. S., Natarajan, V., Harijith, A. Tags: Thorax Paediatric lung disease Source Type: research

Novel KLF4-FOXO1 Interactome in Lung Fibroblasts:Regulator of Myofibroblasts in Hyperoxia-Induced Lung Injury
Conclusion: Our data unveil a novel Klf4-FoxO1 axis in lung fibroblasts that could promote matrix remodeling and lung growth arrest in lungs with BPD.
Source: European Respiratory Journal - October 28, 2020 Category: Respiratory Medicine Authors: Hirani, D., Koch, M., Mohr, J., Vohlen, C., Nayakanti, S., Grimm, C., Schweiger, M.-R., Georgomanolis, T., Pullamsetti, S., Dötsch, J., Alejandre Alcazar, M. A. Tags: Lung and airway developmental biology Source Type: research

14-3-3 β Is necessary in the regulation of polarization and directional migration of alveolar myofibroblasts by lipopolysaccharide.
Conclusions:Taken together, our findings suggest that LPS exposure may increase RhoA activity of myofibroblasts by TGF-α/EGFR/14-3-3β signaling pathway, and then disturb myofibroblasts polarization and directional migration. PMID: 31920140 [PubMed - as supplied by publisher]
Source: Experimental Lung Research - January 12, 2020 Category: Respiratory Medicine Tags: Exp Lung Res Source Type: research

Krüppel-like factor 4 (Klf4) is a novel regulator of neonatal lung fibroblast homeostasis and reduced in hyperoxia-induced lung injury
Conclusion: We identify Klf4 as a novel key regulator of neonatal lung fibroblast homeostasis. Loss of Klf4 is intimately linked to myofibroblast activation, fibrosis and migration, eventually reducing thereby alveolar formation and contributing to the pathogeneis of BPD.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Hirani, D., Koch, M., Dinger, K., Mohr, J., Vohlen, C., Klaudt, C., Dötsch, J., Alejandre Alcazar, M. A. Tags: Lung and airway developmental biology Source Type: research

Role of TREM1-Ripk3 axis in hyperoxia induced lung injury in neonates.
Hyperoxia-induced lung injury (HALI) is one of the major contributor to the development of bronchopulmonary dysplasia (BPD), a devastating lung disease in premature infants, the mechanisms of which are not fully characterized. Here we report that the triggering receptor expressed on myeloid cells 1 (TREM-1) is upregulated in hyperoxia exposed neonatal mice lungs as well as in human neonatal lungs with respiratory distress syndrome (RDS) and BPD as an adaptive response to survive hyperoxia. Inhibition of TREM-1 function using siRNA approach or deletion of TREM-1 gene in mice showed increased alveolar damage and mortality of...
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Syed, M. A., Shah, D., Bhandari, V. Tags: Lung and airway developmental biology Source Type: research

Gene regulatory roles for lysyl oxidases in the context of BPD
We report, for the first time a transcriptome-wide analysis of gene regulation by lysyl oxidases. In the context of primary mouse lung fibroblasts, siRNA knockdown of Lox, Loxl1, and Loxl2 deregulated the expression of 134, 3,761 and 3,554 genes, respectively. Identified lysyl oxidases target-genes relevant to lung development and BPD included Mmp3, Mmp9, Eln, Rarres1, Gdf10, Ifnb1, Cxcl2, and Cxcl9. The expression of target-genes in vivo correlated with the lysyl oxidases expression in a mouse model of BPD. Moreover, using BAPN, we demonstrated that the transcriptional regulation by lysyl oxidases was independent of catal...
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Mizikova, I., Palumbo, F., Morty, R., Seeger, W. Tags: Lung and Airway Developmental Biology Source Type: research

A role for the accessory type III transforming growth factor {beta} receptor (Tgfbr3) in lung alveolarisation
Bronchopulmonary dysplasia (BPD) is a common complication of premature birth, characterised by arrested secondary septation. Molecular mechanisms of arrested secondary septation are not known. Members of the transforming growth factor (TGF)-β growth factor superfamily are accredited with key roles in lung development and BPD. We profiled lung expression of the TGF-β signaling machinery in mice in a hyperoxia-based BPD model, and detected a down-regulation Tgfbr3 expression. Using laser-capture microdissection, Tgfbr3 mRNA expression was reduced in both the lung vascular and parenchymal compartments in response to...
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Pozarska, A., Niess, G., Seeger, W., Morty, R. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research

Inhibition of RPTOR Prevents Hyperoxia-induced Lung Injury by Enhancing Autophagy and Reducing Apoptosis in Neonatal Mice.
Abstract Administration of supplemental oxygen remains a critical clinical intervention for survival of preterm infants with respiratory failure. However, prolonged exposure to hyperoxia can augment pulmonary damage, resulting in developmental lung diseases embodied as hyperoxia-induced acute lung injury (HALI) and bronchopulmonary dysplasia (BPD). We sought to investigate the role of autophagy in hyperoxia-induced apoptotic cell death in developing lungs. We identified increased autophagy signaling in hyperoxia exposed MLE-12 cells, freshly-isolated fetal Type II alveolar epithelial cells, lungs of newborn (NB) w...
Source: Am J Respir Cell Mol... - July 1, 2016 Category: Respiratory Medicine Authors: Angara S, Syed M, Das P, Janér C, Pryhuber G, Rahman A, Andersson S, Homer RJ, Bhandari V Tags: Am J Respir Cell Mol Biol Source Type: research

The p66Shc adapter protein regulates the morphogenesis and epithelial maturation of fetal mouse lungs
Many signaling pathways are mediated by Shc adapter proteins that, in turn, are expressed as three isoforms with distinct functions. The p66Shc isoform antagonizes proliferation, regulates oxidative stress, and mediates apoptosis. It is highly expressed in the canalicular but not the later stages of mouse lung development, and its expression persists in bronchopulmonary dysplasia, a chronic disease associated with premature birth. These observations suggest that p66Shc has a developmental function. However, constitutive p66Shc deletion yields no morphological phenotype, and the structure of the Shc gene precludes its induc...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2014 Category: Respiratory Medicine Authors: Lee, M. K., Smith, S. M., Banerjee, M. M., Li, C., Minoo, P., Volpe, M. V., Nielsen, H. C. Tags: ARTICLES Source Type: research

The p66Shc adapter protein regulates the morphogenesis and epithelial maturation of fetal mouse lungs.
Abstract Many signaling pathways are mediated by Shc adapter proteins which, in turn, are expressed as three isoforms with distinct functions. The p66(Shc) isoform antagonizes proliferation, regulates oxidative stress, and mediates apoptosis. It is highly expressed in the canalicular but not the later stages of mouse lung development, and its expression persists in bronchopulmonary dysplasia, a chronic disease associated with premature birth. These observations suggest that p66(Shc) has a developmental function. However, constitutive p66(Shc) deletion yields no morphologic phenotype, and the structure of the Shc g...
Source: Am J Physiol Lung Ce... - December 27, 2013 Category: Respiratory Medicine Authors: Lee MK, Smith SM, Banerjee MM, Li C, Minoo P, Volpe MV, Nielsen HC Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research