Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8270707 | Free Radical Biology and Medicine | 2014 | 7 Pages |
Abstract
Aldehyde dehydrogenase 3A1 (ALDH3A1), an ALDH superfamily member, catalyzes the oxidation of reactive aldehydes, highly toxic components of cigarette smoke (CS). Even so, the role of ALDH3A1 in CS-induced cytotoxicity and DNA damage has not been examined. Among all of the ALDH superfamily members, ALDH3A1 mRNA levels showed the greatest induction in response to CS extract (CSE) exposure of primary human bronchial epithelial cells (HBECs). ALDH3A1 protein accumulation was accompanied by increased ALDH enzymatic activity in CSE-exposed immortalized HBECs. The effects of overexpression or suppression of ALDH3A1 on CSE-induced cytotoxicity and DNA damage (γH2AX) were evaluated in cultured immortalized HBECs. Enforced expression of ALDH3A1 attenuated cytotoxicity and downregulated γH2AX. SiRNA-mediated suppression of ALDH3A1 blocked ALDH enzymatic activity and augmented cytotoxicity in CSE-exposed cells. Our results suggest that the availability of ALDH3A1 is important for cell survival against CSE in HBECs.
Keywords
LPODNA interstrand crosslinkALDH3A1FANCD2HBECICLDDRCSE4-HNEAHRALDHCDK4-hydroxy-2-nonenalPIKKMTTSmall interfering RNAROSsiRNADNA damagealdehyde dehydrogenaseReactive aldehydesCOPDChronic obstructive pulmonary diseaseCigarette smokeFree radicalsSODAirway epithelial cellsCytotoxicitySuperoxide dismutasecigarette smoke extractDNA damage responseLipid peroxidationFanconi anemiacyclin-dependent kinaseReactive oxygen speciesaryl hydrocarbon receptor
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Authors
Jun-Ho Jang, Shannon Bruse, Yushi Liu, Veronica Duffy, Chunyu Zhang, Nathaniel Oyamada, Scott Randell, Akiko Matsumoto, David C. Thompson, Yong Lin, Vasilis Vasiliou, Yohannes Tesfaigzi, Toru Nyunoya,