Protein S is Protective in Acute Lung Injury by Inhibiting Cell Apoptosis
Autor: | Haruko Saiki, Taro Yasuma, Atsuro Takeshita, Kota Nishihama, Masaaki Toda, Esteban C. Gabazza, Kentaro Fujiwara, Tetsu Kobayashi, Hajime Fujimoto, Prince Baffour Tonto, Corina N. D’Alessandro-Gabazza, Tomohito Okano, Kentaro Asayama |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Lipopolysaccharides Male Lipopolysaccharide MAP Kinase Signaling System Acute Lung Injury Lung injury Neuroprotection Catalysis Protein S Article Proinflammatory cytokine lcsh:Chemistry Inorganic Chemistry 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Erk1/2 Medicine Animals Humans Physical and Theoretical Chemistry lcsh:QH301-705.5 Molecular Biology Spectroscopy signal pathway Lung biology business.industry Kinase Organic Chemistry lipopolysaccharide apoptosis General Medicine respiratory system Computer Science Applications Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure lcsh:Biology (General) lcsh:QD1-999 chemistry Apoptosis 030220 oncology & carcinogenesis biology.protein Cancer research business |
Zdroj: | International Journal of Molecular Sciences International Journal of Molecular Sciences, Vol 20, Iss 5, p 1082 (2019) Volume 20 Issue 5 |
ISSN: | 1422-0067 |
Popis: | Acute lung injury is a fatal disease characterized by inflammatory cell infiltration, alveolar-capillary barrier disruption, protein-rich edema, and impairment of gas exchange. Protein S is a vitamin K-dependent glycoprotein that exerts anticoagulant, immunomodulatory, anti-inflammatory, anti-apoptotic, and neuroprotective effects. The aim of this study was to evaluate whether human protein S inhibits cell apoptosis in acute lung injury. Acute lung injury in human protein S transgenic and wild-type mice was induced by intratracheal instillation of lipopolysaccharide. The effect of human protein S on apoptosis of lung tissue cells was evaluated by Western blotting. Inflammatory cell infiltration, alveolar wall thickening, myeloperoxidase activity, and the expression of inflammatory cytokines were reduced in human protein S transgenic mice compared to the wild-type mice after lipopolysaccharide instillation. Apoptotic cells and caspase-3 activity were reduced while phosphorylation of extracellular signal-regulated kinase was enhanced in the lung tissue from human protein S transgenic mice compared to wild-type mice after lipopolysaccharide instillation. The results of this study suggest that human protein S is protective in lipopolysaccharide-induced acute lung injury by inhibiting apoptosis of lung cells. |
Databáze: | OpenAIRE |
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