Inhibition of gene expression of heparin-binding epidermal growth factor-like growth factor by extracellular superoxide dismutase in rat aortic smooth muscle cells |
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Authors: | Nishimura Masashi Ookawara Tomomi Eguchi Hironobu Fujiwara Noriko Yoshihara Daisaku Yasuda Jun Mimura Osamu Suzuki Keiichiro |
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Affiliation: | a Department of Ophthalmology, Hyogo College of Medicine, Hyogo, Japanb Department of Biochemistry, Hyogo College of Medicine, Hyogo, Japan |
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Abstract: | 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. |
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Keywords: | EC-SOD Atherosclerosis HB-EGF EGFR signaling ROS |
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