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Peroxiredoxin 6 protects lung epithelial type II cells against H 2 O 2 ‐induced oxidative stress
Author(s) -
Wang Yan,
Feinstein Sheldon I.,
Manevich Yefim,
Fisher Aron B.
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.a1179-d
Subject(s) - oxidative stress , propidium iodide , annexin , apoptosis , chemistry , microbiology and biotechnology , lipid peroxidation , viability assay , cell , programmed cell death , biochemistry , biology
Peroxiredoxin 6 (Prdx6) is a novel antioxidant enzyme that protects against lung injury associated with oxidative stress. Lung alveolar epithelial type II cells (AECII) play a pivotal role in lung fluid balance, the inflammatory response, and surfactant secretion. The present study investigated the response to H 2 O 2 exposure (50–500 μM for 24 h) of AECII that were isolated from wild type (WT) or Prdx null or transgenic overexpressor (Tg) mouse lungs. H 2 O 2 (250 μM) in WT cells induced Prdx6 protein expression by ~250% during the 24 h treatment period. H 2 O 2 exposure of WT cells resulted in a dose‐dependent decrease in cell viability (calcein fluorescence), increased apoptosis (annexin V binding), increased cytotoxicity (propidium iodide uptake), and increased lipid peroxidation (DPPP fluorescence). Prdx6 null cells showed increased cell injury compared to WT cells while overexpressing Tg cells showed protection against these indices of cell injury associated with H 2 O 2 treatment. Thus, deletion of Prdx6 from AECII cells increased their susceptibility to H 2 O 2 ‐induced oxidative stress while Prdx6 overexpression was protective. We propose that Prdx6 protects against cell injury with oxidative stress through its ability to reduce cell membrane lipid hydroperoxides [HL 79063].