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p53/PUMA expression in human pulmonary fibroblasts mediates cell activation and migration in silicosis

Wei Wang1,2,3, Haijun Liu2,4, Xiaoniu Dai2

  • 1Department of Respiratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China.

Scientific Reports
|November 19, 2015
PubMed

Insights

Silica (SiO2) exposure triggers lung inflammation and fibrosis by activating macrophages. This study reveals p53 and PUMA proteins are key mediators in silica-induced fibroblast activation and migration, offering potential therapeutic targets for silicosis.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Toxicology

Background:

  • Silica (SiO2) inhalation causes lung inflammation and fibrosis.
  • Activated macrophages release monocyte chemotactic protein 1 (MCP-1), inducing fibroblast proliferation and migration.
  • The precise molecular mechanisms downstream of MCP-1 in pulmonary fibroblasts leading to fibrosis are not fully understood.

Purpose of the Study:

  • To investigate the role of p53 in silica-induced pulmonary fibrosis.
  • To elucidate the upstream molecular mechanisms regulating p53 expression.
  • To determine the functional effects of p53 on fibroblast proliferation and migration.

Main Methods:

  • Primary adult human pulmonary fibroblasts were cultured and treated with SiO2.
  • Western blotting was used to assess protein levels of p53 and PUMA.
  • Mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways were investigated.
  • RNA interference (RNAi) was employed to target p53 and PUMA.

Main Results:

  • SiO2 treatment led to a significant and sustained increase in p53 and PUMA protein levels.
  • MAPK and PI3K signaling pathways were implicated in SiO2-induced p53 and PUMA expression.
  • Targeting p53 and PUMA via RNAi inhibited SiO2-induced fibroblast activation and migration.

Conclusions:

  • A direct link exists between SiO2-induced p53/PUMA expression in pulmonary fibroblasts and enhanced cell migration.
  • p53 and PUMA play critical roles in the fibrotic response to silica exposure.
  • Targeting the p53/PUMA pathway presents a potential therapeutic strategy for treating silicosis.

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