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Prolonged cigarette smoke exposure decreases heme oxygenase‐1 and alters Nrf2 and Bach1 expression in human macrophages: Roles of the MAP kinases ERK 1/2 and JNK
Author(s) -
Goven D.,
Boutten A.,
Leçon-Malas V.,
Boczkowski J.,
Bonay M.
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.10.010
Subject(s) - heme oxygenase , heme , cigarette smoke , kinase , mapk/erk pathway , microbiology and biotechnology , chemistry , oxygenase , hmox1 , biochemistry , biology , toxicology , gene , enzyme
Tobacco may be involved in the decreased macrophage heme oxygenase‐1 (HO‐1) expression described in smoking‐induced severe emphysema, via the nuclear factor erythroid 2‐related factor 2 (Nrf2)/Kelch‐like ECH‐associated protein 1 (Keap1)–BTB and CNC homology 1, basic leucine zipper transcription factor 1 (Bach1) pathway. We assessed in vitro effects of cigarette smoke condensate (CS) in the human monocyte/macrophage cell line (THP‐1). CS exposure led to increased HO‐1 and nuclear Nrf2 expression (6 h) followed by decreased HO‐1 expression concomitantly with nuclear Nrf2/Bach1 ratio decrease (72 h). CS‐induced mitogen‐activated protein kinase (MAPK) phosphorylation. Extracellular‐signal‐regulated kinase 1/2 (ERK 1/2 ) and c‐Jun NH2‐terminal kinase (JNK) inhibition completely abrogated CS effects on HO‐1 expression and nuclear Nrf2/Bach1 translocation. These results suggest that ERK 1/2 and JNK are involved in CS‐induced biphasic HO‐1 expression by a specific regulation of Nrf2/Keap1–Bach1.