Abstract |
Extracellular alkalosis induced phosphorylation of extracellular signal-regulated kinase (ERK) and enhanced serum-induced ERK phosphorylation in cultured rat aortic smooth muscle cells. While extracellular alkalinization increased verapamil-sensitive (45)Ca(2+) uptake into the cells, ERK phosphorylation induced by extracellular alkalosis was not affected by verapamil. On the other hand, probes for oxidant signaling, such as superoxide dismutase, 4,5-dihydroxy-1,3-benzene-disulfonic acid, a cell-permeable antioxidant, and diphenyliodonium, a NADPH oxidase inhibitor, inhibited extracellular alkalosis-induced phosphorylation of ERK. These results suggest that activation of ERK induced by extracellular alkalosis is not dependent on transplasmalemmal Ca(2+) entry but is caused by reactive oxygen species derived from an activation of NADPH oxidase.
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Authors | Shinji Susa, Ichiro Wakabayashi |
Journal | FEBS letters
(FEBS Lett)
Vol. 554
Issue 3
Pg. 399-402
(Nov 20 2003)
ISSN: 0014-5793 [Print] England |
PMID | 14623101
(Publication Type: Journal Article)
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Chemical References |
- Onium Compounds
- Reactive Oxygen Species
- 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
- NADP
- Superoxide Dismutase
- NADPH Oxidases
- Mitogen-Activated Protein Kinases
- Tetradecanoylphorbol Acetate
- HEPES
- Calcium
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Topics |
- 1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
(pharmacology)
- Animals
- Aorta
(cytology)
- Calcium
(chemistry, metabolism)
- Enzyme Activation
- HEPES
(pharmacology)
- Hydrogen-Ion Concentration
- Male
- Mitogen-Activated Protein Kinases
(metabolism)
- Muscle, Smooth, Vascular
(cytology, metabolism)
- NADP
(metabolism)
- NADPH Oxidases
(antagonists & inhibitors, metabolism)
- Onium Compounds
(pharmacology)
- Phosphorylation
- Rats
- Rats, Wistar
- Reactive Oxygen Species
(antagonists & inhibitors, metabolism)
- Superoxide Dismutase
(metabolism, pharmacology)
- Tetradecanoylphorbol Acetate
(pharmacology)
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