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An oxidized extracellular oxidation-reduction state increases Nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation.

Publication ,  Journal Article
Stanic, B; Katsuyama, M; Miller, FJ
Published in: Arterioscler Thromb Vasc Biol
November 2010

OBJECTIVE: To examine the effect of an oxidized extracellular oxidation-reduction (redox) state (E(h)) on the expression of NADPH oxidases in vascular cells. METHODS AND RESULTS: The generation of reactive oxygen species by NADPH oxidase (Nox)-based NADPH oxidases activates redox-dependent signaling pathways and contributes to the development of "oxidative stress" in vascular disease. An oxidized plasma redox state is associated with cardiovascular disease in humans; however, the cellular mechanisms by which the extracellular redox state may cause disease are not known. Aortic segments and cultured aortic smooth muscle cells were exposed to E(h) between -150 mV (reduced) and 0 mV (oxidized) by altering the concentration of cysteine and its disulfide, cystine, the predominant redox couple in plasma. A more oxidized E(h) increased the expression of Nox1 and resulted in Nox1-dependent proliferation of smooth muscle cells. Oxidized E(h) rapidly induced epidermal growth factor receptor phosphorylation via shedding of epidermal growth factor-like ligands from the plasma membrane and caused extracellular signal-regulated kinase 1/2-dependent phosphorylation of the transcription factors activating transcription factor-1 and cAMP-response element-binding protein. Inhibition of epidermal growth factor receptor or extracellular signal-regulated kinase 1/2 activation, or addition of small interference RNA to activating transcription factor-1, prevented the increase in Nox1 expression. CONCLUSIONS: Our results identify a novel mechanism by which extracellular oxidative stress increases expression and activity of Nox1 NADPH oxidase and contributes to vascular disease.

Duke Scholars

Published In

Arterioscler Thromb Vasc Biol

DOI

EISSN

1524-4636

Publication Date

November 2010

Volume

30

Issue

11

Start / End Page

2234 / 2241

Location

United States

Related Subject Headings

  • Signal Transduction
  • Oxidative Stress
  • Oxidation-Reduction
  • NADPH Oxidase 1
  • NADH, NADPH Oxidoreductases
  • Myocytes, Smooth Muscle
  • Muscle, Smooth, Vascular
  • Models, Animal
  • Mice, Inbred C57BL
  • Mice
 

Citation

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Stanic, B., Katsuyama, M., & Miller, F. J. (2010). An oxidized extracellular oxidation-reduction state increases Nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation. Arterioscler Thromb Vasc Biol, 30(11), 2234–2241. https://doi.org/10.1161/ATVBAHA.110.207639
Stanic, Bojana, Masato Katsuyama, and Francis J. Miller. “An oxidized extracellular oxidation-reduction state increases Nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation.Arterioscler Thromb Vasc Biol 30, no. 11 (November 2010): 2234–41. https://doi.org/10.1161/ATVBAHA.110.207639.
Stanic, Bojana, et al. “An oxidized extracellular oxidation-reduction state increases Nox1 expression and proliferation in vascular smooth muscle cells via epidermal growth factor receptor activation.Arterioscler Thromb Vasc Biol, vol. 30, no. 11, Nov. 2010, pp. 2234–41. Pubmed, doi:10.1161/ATVBAHA.110.207639.

Published In

Arterioscler Thromb Vasc Biol

DOI

EISSN

1524-4636

Publication Date

November 2010

Volume

30

Issue

11

Start / End Page

2234 / 2241

Location

United States

Related Subject Headings

  • Signal Transduction
  • Oxidative Stress
  • Oxidation-Reduction
  • NADPH Oxidase 1
  • NADH, NADPH Oxidoreductases
  • Myocytes, Smooth Muscle
  • Muscle, Smooth, Vascular
  • Models, Animal
  • Mice, Inbred C57BL
  • Mice