Autor: |
Prince Baffour Tonto, Taro Yasuma, Tetsu Kobayashi, Corina N. D’Alessandro-Gabazza, Masaaki Toda, Haruko Saiki, Hajime Fujimoto, Kentaro Asayama, Kentaro Fujiwara, Kota Nishihama, Tomohito Okano, Atsuro Takeshita, Esteban C. Gabazza |
Jazyk: |
angličtina |
Rok vydání: |
2019 |
Předmět: |
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Zdroj: |
International Journal of Molecular Sciences, Vol 20, Iss 5, p 1082 (2019) |
Druh dokumentu: |
article |
ISSN: |
1422-0067 |
DOI: |
10.3390/ijms20051082 |
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: |
Directory of Open Access Journals |
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