Inhibition of gene expression of heparin-binding epidermal growth factor-like growth factor by extracellular superoxide dismutase in rat aortic smooth muscle cells

Both extracellular superoxide dismsutase (EC-SOD) and heparin binding EGF like growth factor (HB-EGF) are produced in smooth muscle cells of the arterial wall, and are thought to play pathological roles in atherosclerosis with heparin binding characteristics. EC-SOD treatment clearly reduced the H2O...

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Bibliographic Details
Published in:Free radical research 2006-06, Vol.40 (6), p.589-595
Main Authors: Nishimura, Masashi, Ookawara, Tomomi, Eguchi, Hironobu, Fujiwara, Noriko, Yoshihara, Daisaku, Yasuda, Jun, Mimura, Osamu, Suzuki, Keiichiro
Format: Article
Language:English
Subjects:
Animals
Aorta - cytology
Atherosclerosis
Cells, Cultured
EC-SOD
EGFR signaling
Epidermal Growth Factor - genetics
Extracellular Space - metabolism
Gene Expression Regulation - drug effects
HB-EGF
Heparin - pharmacology
Heparin-binding EGF-like Growth Factor
Intercellular Signaling Peptides and Proteins
Intracellular Space - metabolism
Mice
Muscle, Smooth, Vascular - cytology
Myocytes, Smooth Muscle - drug effects
Myocytes, Smooth Muscle - metabolism
Rats
Reactive Oxygen Species - metabolism
Recombinant Proteins - pharmacology
ROS
Superoxide Dismutase - metabolism
Superoxide Dismutase - pharmacology
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Summary:Both extracellular superoxide dismsutase (EC-SOD) and heparin binding EGF like growth factor (HB-EGF) are produced in smooth muscle cells of the arterial wall, and are thought to play pathological roles in atherosclerosis with heparin binding characteristics. EC-SOD treatment clearly reduced the H2O2 induced expression of HB-EGF in rat aortic smooth muscle cells (RASMC). EC-SOD also inhibited the induction of HB-EGF by 12-O-tetradecanoylphorbol-13-acetate (TPA) in RASMC by 60%. Both H2O2 and TPA increased intracellular ROS levels, and EC-SOD inhibited ROS generation only for the case of H2O2 but not TPA. Treatment of the cells with heparin alone decreased HB-EGF expression by 20%, whereas EC-SOD alone and a co-incubation with EC-SOD and heparin suppressed the induction by 60 and 70%, respectively. These results suggest that EC-SOD is related to the EGF signaling in two ways, competition for HSPG with HB-EGF and as an ROS scavenger.
ISSN:1071-5762
1029-2470
DOI:10.1080/10715760600615094