CO/HO-1 Induces NQO-1 Expression via Nrf2 Activation
Immune Network
;
: 376-382, 2011.
Article
in English
| WPRIM
| ID: wpr-60136
ABSTRACT
BACKGROUND:
Carbon monoxide (CO) is a cytoprotective and homeostatic molecule with important signaling capabilities in physiological and pathophysiological situations. CO protects cells/tissues from damage by free radicals or oxidative stress. NAD(P)Hquinone oxidoreductase (NQO1) is a highly inducible enzyme that is regulated by the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway, which is central to efficient detoxification of reactive metabolites and reactive oxygen species (ROS).METHODS:
We generated NQO1 promoter construct. HepG2 cells were treated with CO Releasing Molecules-2 (CORM-2) or CO gas and the gene expressions were measured by RT-PCR, immunoblot, and luciferase assays.RESULTS:
CO induced expression of NQO1 in human hepatocarcinoma cell lines by activation of Nrf2. Exposure of HepG2 cells to CO resulted in significant induction of NQO1 in dose- and time-dependent manners. Analysis of the NQO1 promoter indicated that an antioxidant responsible element (ARE)-containing region was critical for the CO-induced Nrf2-dependent increase of NQO1 gene expression in HepG2 cells.CONCLUSION:
Our results suggest that CO-induced Nrf2 increases the expression of NQO1 which is well known to detoxify reactive metabolites and ROS.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Carbon Monoxide
/
Gene Expression
/
Cell Line
/
Reactive Oxygen Species
/
Oxidative Stress
/
Response Elements
/
Heme Oxygenase-1
/
Hep G2 Cells
/
Free Radicals
/
Luciferases
Limits:
Humans
Language:
English
Journal:
Immune Network
Year:
2011
Type:
Article
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