Aldehyde dehydrogenase 3A1 protects airway epithelial cells from cigarette smoke-induced DNA damage and cytotoxicity

被引：46

作者：

Fang, Jun-Ho ^{[1
,2
,3
]}

Bruse, Shannon ^{[3
]}

Liu, Yushi ^{[3
]}

Duffy, Veronica ^{[3
]}

Zhang, Chunyu ^{[3
]}

Oyamada, Nathaniel ^{[3
]}

Randell, Scott ^{[4
]}

Matsumoto, Akiko ^{[5
]}

Thompson, David C. ^{[5
]}

Lin, Yong ^{[3
]}

Vasiliou, Vasilis ^{[5
]}

Tesfaigzi, Yohannes ^{[3
]}

Nyunoya, Toru ^{[1
,2
,3
]}

机构：

[1] Univ New Mexico, Dept Internal Med, Div Pulm Crit Care & Sleep Med, Albuquerque, NM 87131 USA

[2] New Mexico VA Hlth Care Syst, Albuquerque, NM 87108 USA

[3] Lovelace Resp Res Inst, COPD Program, Albuquerque, NM 87108 USA

[4] Univ N Carolina, Dept Cell & Mol Physiol, Chapel Hill, NC 27599 USA

[5] Univ Colorado Denver, Dept Pharmacol, Aurora, CO 80045 USA

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2014年 / 68卷

关键词：

Cigarette smoke; Airway epithelial cells; Chronic obstructive pulmonary disease; ALDH3A1; Reactive aldehydes; DNA damage; Cytotoxicity; FANCD2; Free radicals; OBSTRUCTIVE PULMONARY-DISEASE; LIPID-PEROXIDATION; DOWN-REGULATION; CELLULAR SENESCENCE; GENE-EXPRESSION; ALDH3A1; FIBROBLASTS; INHIBITION; GAMMA-H2AX; ACTIVATION;

D O I：

10.1016/j.freeradbiomed.2013.11.028

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 (gamma H2AX) were evaluated in cultured immortalized HBECs. Enforced expression of ALDH3A1 attenuated cytotoxicity and down-regulated gamma H2AX. 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. Published by Elsevier Inc.

引用

页码：80 / 86

页数：7

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