Rad9 is upregulated and plays protective roles in an acute lung injury model

Biochem Biophys Res Commun. 2008 Nov 21;376(3):590-4. doi: 10.1016/j.bbrc.2008.09.058. Epub 2008 Sep 20.

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.

MeSH terms

  • Animals
  • Bleomycin / toxicity
  • Cell Cycle / genetics
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / physiology*
  • Disease Models, Animal
  • Gene Silencing
  • Hydrogen Peroxide / toxicity
  • Mice
  • Pulmonary Alveoli / drug effects
  • Pulmonary Alveoli / metabolism
  • Pulmonary Alveoli / pathology
  • RNA, Small Interfering / genetics
  • Respiratory Distress Syndrome / chemically induced
  • Respiratory Distress Syndrome / genetics*
  • Respiratory Distress Syndrome / pathology
  • Respiratory Mucosa / drug effects
  • Respiratory Mucosa / metabolism
  • Respiratory Mucosa / pathology
  • Up-Regulation

Substances

  • Cell Cycle Proteins
  • RNA, Small Interfering
  • Bleomycin
  • rad9 protein
  • Hydrogen Peroxide