Premium
Wood Smoke Extract Promotes Both Proliferation and Apoptosis in Rat Alveolar Epithelial Type II Cells: Role of Oxidative Stress and Heme Oxygenase‐1
Author(s) -
Liu PoLen,
Liu YuJu,
Chen YuhLien,
Kou Yu Ru
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1438-c
Subject(s) - oxidative stress , heme oxygenase , apoptosis , heme , microbiology and biotechnology , chemistry , cigarette smoke , biology , biochemistry , enzyme , toxicology
We investigated the role of oxidative stress and heme oxygenase‐1 (HO‐1, a stress protein) in the responses of rat alveolar epithelial type II (AEII) cells to wood smoke extract (SE). Exposure of AEII cells to SE (60 μg/ml) increased intracellular reactive oxygen species (ROS), expression of HO‐1, and total and dead cell numbers. SE promoted proliferation as indicated by increases in viable cell number, DNA synthesis, expression of cyclin D1, and the percentage of cells in S and G2/M phase of the cell cycle. SE also accelerated apoptosis as indicated by nuclear translocation of apoptosis‐inducing factor and endonuclease G, caspase‐3 activation, and enhanced DNA fragmentation. Pretreatment with N‐acetylcysteine (an antioxidant) prevented SE‐induced increases in intracellular ROS, up‐regulation of HO‐1, proliferation, and apoptosis. HO‐1 gene silencing or tin protoporphyrin‐IX (a HO‐1 inhibitor) prevented the proliferation, but further aggravated the apoptosis. Conversely, cobalt‐protoporphyrin‐IX (a HO‐1 enhancer) further augmented the proliferation, but suppressed the apoptosis. These results suggest that 1) SE causes oxidative stress, which promotes both proliferation and apoptosis in rat AEII cells and 2) this oxidative stress up‐regulates HO‐1, which mediates SE‐induced proliferation, but counteracts SE‐induced apoptosis (Supported by NSC 93‐2320‐B‐010‐028).