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10.1186/s12931-015-0275-6 http://scihub22266oqcxt.onion/10.1186/s12931-015-0275-6 C4574227!4574227 !26377087     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26377087 &cmd=llinks): Failed to open stream: HTTP request failed! 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Activation of Src-dependent Smad3 signaling mediates the neutrophilic inflammation and oxidative stress in hyperoxia-augmented ventilator-induced lung injury |pdf=|usr=}}{{26377087 }} gab.com Text Activation of Src-dependent Smad3 signaling mediates the neutrophilic inflammation and oxidative stress in hyperoxia-augmented ventilator-induced lung injury JO: Respir Res http://www.kidney.de/pget.php?&tw=1&pmid=26377087 #FOAvip BACKGROUND: Mechanical ventilation and concomitant administration of hyperoxia in patients with acute respiratory distress syndrome can damage the alveolar epithelial and capillary endothelial barrier by producing inflammatory cytokines and reactive oxygen species. The Src tyrosine kinase and Smad3 are crucial inflammatory regulators used for ventilator-induced lung injury (VILI). The mechanisms regulating interactions between high-tidal-volume mechanical ventilation, hyperoxia, and acute lung injury (ALI) are unclear. We hypothesized that high-tidal-volume mechanical stretches and hyperoxia augment lung inflammation through upregulation of the Src and Smad3 pathways. METHODS: Wild-type or Src-deficient C57BL/6 mice, aged between 6 and 8 weeks, were exposed to high-tidal-volume (30 mL/kg) ventilation with room air or hyperoxia for 1-4 h after 2-mg/kg Smad3 inhibitor (SIS3) administration. Nonventilated mice were used as control subjects. RESULTS: We observed that the addition of hyperoxia to high-tidal-volume mechanical ventilation further induced microvascular permeability, neutrophil infiltration, macrophage inflammatory protein-2 and matrix metalloproteinase-9 (MMP-9) production, malondialdehyde, nicotinamide adenine dinucleotide phosphate oxidase activity, MMP-9 mRNA expression, hypoxemia, and Src and Smad3 activation (P < 0.05). Hyperoxia-induced augmentation of VILI was attenuated in Src-deficient mice and mice with pharmacological inhibition of Smad3 activity by SIS3 (P < 0.05). Mechanical ventilation of Src-deficient mice with hyperoxia further reduced the activation of Smad3. CONCLUSIONS: Our data suggest that hyperoxia-increased high-tidal-volume ventilation-induced ALI partially depends on the Src and Smad3 pathways. Twit Text FOAVip Activation of Src-dependent Smad3 signaling mediates the neutrophilic inflammation and oxidative stress in hyperoxia-augmented ventilator-induced lung injury ????Respir Res http://www.kidney.de/pget.php?&tw=1&pmid=26377087 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26377087 #FOAvip English Wikipedia <ref>{{Cite pmid|26377087 }}</ref> Activation of Src-dependent Smad3 signaling mediates the neutrophilic inflammation and oxidative stress in hyperoxia-augmented ventilator-induced lung injury #MMPMID26377087 Li LF ; Lee CS ; Liu YY ; Chang CH ; Lin CW ; Chiu LC ; Kao KC ; Chen NH ; Yang CT Respir Res 2015[Sep]; 16 (1 ): 112 PMID26377087 show ga BACKGROUND: Mechanical ventilation and concomitant administration of hyperoxia in patients with acute respiratory distress syndrome can damage the alveolar epithelial and capillary endothelial barrier by producing inflammatory cytokines and reactive oxygen species. The Src tyrosine kinase and Smad3 are crucial inflammatory regulators used for ventilator-induced lung injury (VILI). The mechanisms regulating interactions between high-tidal-volume mechanical ventilation, hyperoxia, and acute lung injury (ALI) are unclear. We hypothesized that high-tidal-volume mechanical stretches and hyperoxia augment lung inflammation through upregulation of the Src and Smad3 pathways. METHODS: Wild-type or Src-deficient C57BL/6 mice, aged between 6 and 8 weeks, were exposed to high-tidal-volume (30 mL/kg) ventilation with room air or hyperoxia for 1-4 h after 2-mg/kg Smad3 inhibitor (SIS3) administration. Nonventilated mice were used as control subjects. RESULTS: We observed that the addition of hyperoxia to high-tidal-volume mechanical ventilation further induced microvascular permeability, neutrophil infiltration, macrophage inflammatory protein-2 and matrix metalloproteinase-9 (MMP-9) production, malondialdehyde, nicotinamide adenine dinucleotide phosphate oxidase activity, MMP-9 mRNA expression, hypoxemia, and Src and Smad3 activation (P < 0.05). Hyperoxia-induced augmentation of VILI was attenuated in Src-deficient mice and mice with pharmacological inhibition of Smad3 activity by SIS3 (P < 0.05). Mechanical ventilation of Src-deficient mice with hyperoxia further reduced the activation of Smad3. CONCLUSIONS: Our data suggest that hyperoxia-increased high-tidal-volume ventilation-induced ALI partially depends on the Src and Smad3 pathways. |*Oxidative Stress/drug effects [MESH] |*Signal Transduction/drug effects [MESH] |Animals [MESH] |Capillary Permeability [MESH] |Chemokine CXCL2/metabolism [MESH] |Disease Models, Animal [MESH] |Genetic Predisposition to Disease [MESH] |Hyperoxia/*complications [MESH] |Isoquinolines/pharmacology [MESH] |Lung/blood supply/drug effects/*enzymology/immunology/pathology [MESH] |Matrix Metalloproteinase 9/metabolism [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |NADPH Oxidases/metabolism [MESH] |Neutrophil Infiltration [MESH] |Neutrophils/drug effects/*enzymology/immunology [MESH] |Phenotype [MESH] |Pneumonia/enzymology/*etiology/genetics/immunology/pathology/prevention & control [MESH] |Pyridines/pharmacology [MESH] |Pyrroles/pharmacology [MESH] |Respiration, Artificial/*adverse effects [MESH] |Smad3 Protein/antagonists & inhibitors/*metabolism [MESH] |Tidal Volume [MESH] |Ventilator-Induced Lung Injury/enzymology/*etiology/genetics/immunology/pathology/prevention & control [MESH]Activation of Src-dependent Smad3 signaling mediates the neutrophilic (epmc).pdf DeepDyve Pubget Overpricing