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Rad9 is upregulated and plays protective roles in an acute lung injury model |
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| Authors: | Yamamoto Masatsugu Nishiuma Teruaki Kobayashi Kazuyuki Maniwa Yoshimasa Sakashita Akihiro Funada Yasuhiro Kotani Yoshikazu Nishimura Yoshihiro |
| Institution: | a Divisions of Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho, Chuo-ku, Kobe, Hyogo 650-0017, Japan b Divisions of Thoracic Surgery, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho, Chuo-ku, Kobe, Hyogo 650-0017, Japan |
| Abstract: | The Rad9-Hus1-Rad1 protein complex is believed to respond to DNA damage and play important roles in the cell cycle. We studied the role of Rad9 protein in alveolar epithelial cells in the pathogenesis of acute lung injury. In a mouse model of lung injury induced by bleomycin or lipopolysaccharide, Rad9 expression is increased in type II alveolar epithelial cells from the early stage of lung injury. A549 cells and mouse primary alveolar epithelial cells also upregulated Rad9 expression after exposure to bleomycin. Gene silencing of Rad9 using siRNA decreased the G2/M arrest in A549 cells induced by bleomycin and also decreased the survival of A549 cells following exposure to bleomycin and hydrogen peroxide. In conclusion, Rad9 is a signal in the earlier stage of epithelial cell cycle regulation and plays protective roles in alveolar epithelial cells in the pathogenesis of acute lung injury. |
| Keywords: | Acute lung injury Rad9 Lipopolysaccharide Bleomycin Cell cycle arrest |
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