Increase in p21 expression independent of the p53 pathway in bleomycin-induced lung fibrosis

Exp Mol Pathol. 2004 Dec;77(3):231-7. doi: 10.1016/j.yexmp.2004.07.003.

Abstract

Although a number of animal models have been used to study the pathogenesis of lung disease, to date few studies have looked at changed in the expression of cell cycle regulatory genes. We have studied the variation in the expression of p21, p53, p27 and PCNA in bleomycin-induced lung fibrosis using animal mouse models using immuno-histochemistry and gene-expression analysis. No difference in the p53, PCNA and p27 expressions were observed from the bleomycin-induced fibrosis when compared to saline-induced non-fibrotic lungs. Although no difference in nuclear p21 expression was observed, the level of cytoplasmic p21 expression was found to be higher in fibrotic lungs at day 14 after bleomycin injection. p21 expression was found to increase independent of p53 in fibrotic lungs at 14 days after bleomycin induction.

MeSH terms

  • Animals
  • Bleomycin / toxicity*
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Disease Models, Animal
  • Fluorescent Antibody Technique, Indirect
  • Lung / drug effects
  • Lung / metabolism*
  • Lung / pathology
  • Mice
  • Mice, Inbred C57BL
  • Oligonucleotide Array Sequence Analysis
  • Pulmonary Fibrosis / chemically induced
  • Pulmonary Fibrosis / metabolism*
  • Pulmonary Fibrosis / pathology
  • Specific Pathogen-Free Organisms
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Cdkn1a protein, mouse
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Tumor Suppressor Protein p53
  • Bleomycin