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Start Over Author "Thanassopoulou A" Topic ventilator-induced lung injury
2 results on '"Thanassopoulou A"'

1. A critical role for gelsolin in ventilator-induced lung injury.

Author

Maniatis NA, Harokopos V, Thanassopoulou A, Oikonomou N, Mersinias V, Witke W, Orfanos SE, Armaganidis A, Roussos C, Kotanidou A, and Aidinis V

Subjects
Airway Resistance, Animals, Apoptosis, Bronchoalveolar Lavage Fluid cytology, Capillary Permeability, Cytokines metabolism, Gelsolin deficiency, Gelsolin genetics, Lung pathology, Lung Compliance, Mice, Mice, Knockout, Neutrophils pathology, Pulmonary Edema etiology, Pulmonary Edema physiopathology, Pulmonary Edema prevention & control, Stress, Mechanical, Ventilator-Induced Lung Injury etiology, Ventilator-Induced Lung Injury pathology, Ventilator-Induced Lung Injury prevention & control, Gelsolin physiology, High-Frequency Ventilation adverse effects, Ventilator-Induced Lung Injury physiopathology
Abstract

Mechanical ventilation, an essential life-support modality of patients with acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS), exerts its detrimental effects through largely unknown mechanisms. Gelsolin (GSN), an actin-binding protein and a substrate of caspase-3, was recently shown to play a major role in bleomycin- or lipopolysaccharide-induced lung injury. To dissect a possible role of GSN in the pathogenesis of ventilator-induced lung injury (VILI), genetically modified mice lacking GSN expression and wild-type controls underwent mechanical ventilation with high tidal volumes. GSN was found up-regulated in the airways upon VILI, and its genetic ablation led to almost complete disease protection as manifested by reduced edema formation, reduced lung injury, attenuated epithelial apoptosis, diminished cytokine expression, and impaired neutrophil infiltration. GSN fragmentation was shown to be an effector mechanism in VILI-induced apoptosis, while GSN expression was shown to be necessary for efficient neutrophil infiltration, which was found to be a prerequisite for VILI induction in this model. Therefore, intracellular GSN and GSN-mediated responses were shown to be an important player in the pathogenesis of VILI.

Published
2009
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2. A Critical Role for Gelsolin in Ventilator-Induced Lung Injury

Author

Walter Witke, Nikolaos A. Maniatis, Charalambos Roussos, Vaggelis Harokopos, Nikos Oikonomou, Vassilis Aidinis, Apostolos Armaganidis, Vassilis Mersinias, Artemis Thanassopoulou, Anastasia Kotanidou, and Stylianos E. Orfanos

Subjects
Pulmonary and Respiratory Medicine, ARDS, Neutrophils, Ventilator-Induced Lung Injury, medicine.medical_treatment, Clinical Biochemistry, High-Frequency Ventilation, Apoptosis, Pulmonary Edema, Lung injury, Bleomycin, Capillary Permeability, Pathogenesis, Mice, chemistry.chemical_compound, medicine, Animals, Lung, Lung Compliance, Molecular Biology, Gelsolin, Mice, Knockout, Mechanical ventilation, business.industry, Airway Resistance, Cell Biology, respiratory system, medicine.disease, respiratory tract diseases, chemistry, Immunology, Cytokines, Stress, Mechanical, business, Bronchoalveolar Lavage Fluid, Infiltration (medical)
Abstract

Mechanical ventilation, an essential life-support modality of patients with acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS), exerts its detrimental effects through largely unknown mechanisms. Gelsolin (GSN), an actin-binding protein and a substrate of caspase-3, was recently shown to play a major role in bleomycin- or lipopolysaccharide-induced lung injury. To dissect a possible role of GSN in the pathogenesis of ventilator-induced lung injury (VILI), genetically modified mice lacking GSN expression and wild-type controls underwent mechanical ventilation with high tidal volumes. GSN was found up-regulated in the airways upon VILI, and its genetic ablation led to almost complete disease protection as manifested by reduced edema formation, reduced lung injury, attenuated epithelial apoptosis, diminished cytokine expression, and impaired neutrophil infiltration. GSN fragmentation was shown to be an effector mechanism in VILI-induced apoptosis, while GSN expression was shown to be necessary for efficient neutrophil infiltration, which was found to be a prerequisite for VILI induction in this model. Therefore, intracellular GSN and GSN-mediated responses were shown to be an important player in the pathogenesis of VILI.

Published
2009
Full Text
View/download PDF

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