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Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells.

Publication ,  Journal Article
Li, Z; Hyseni, X; Carter, JD; Soukup, JM; Dailey, LA; Huang, Y-CT
Published in: Am J Physiol Cell Physiol
August 2006

Particulate matter (PM) induces oxidative stress and cardiovascular adverse health effects, but the mechanistic link between the two is unclear. We hypothesized that PM enhanced oxidative stress in vascular endothelial cells and investigated the enzymatic sources of reactive oxygen species and their effects on mitogen-activated protein kinase (MAPK) activation and vasoconstriction. We measured the production of extracellular H2O2, activation of extracellular signal-regulated kinases1/2 (ERK1/2) and p38 MAPKs in human pulmonary artery endothelial cells (HPAEC) treated with urban particles (UP; SRM1648), and assessed the effects of H2O2 on vasoconstriction in pulmonary artery ring and isolated perfused lung. Within minutes after UP treatment, HPAEC increased H2O2 production that could be inhibited by diphenyleneiodonium (DPI), apocynin (APO), and sodium azide (NaN3). The water-soluble fraction of UP as well as its two transition metal components, Cu and V, also stimulated H2O2 production. NaN3 inhibited H2O2 production stimulated by Cu and V, whereas DPI and APO inhibited only Cu-stimulated H2O2 production. Inhibitors of other H2O2-producing enzymes, including Nomega-methyl-L-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. DPI but not NaN3 attenuated UP-induced pulmonary vasoconstriction and phosphorylation of ERK1/2 and p38 MAPKs. Knockdown of p47phox gene expression by small interfering RNA attenuated UP-induced H2O2 production and phosphorylation of ERK1/2 and p38 MAPKs. Intravascular administration of H2O2 generated by glucose oxidase increased pulmonary artery pressure. We conclude that UP induce oxidative stress in vascular endothelial cells by activating NAD(P)H oxidase and the mitochondria. The endothelial oxidative stress may be an important mechanism for PM-induced acute cardiovascular health effects.

Duke Scholars

Published In

Am J Physiol Cell Physiol

DOI

ISSN

0363-6143

Publication Date

August 2006

Volume

291

Issue

2

Start / End Page

C357 / C365

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Rabbits
  • Pulmonary Artery
  • Physiology
  • Particle Size
  • Oxidative Stress
  • NADP
  • Mitochondria
  • In Vitro Techniques
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Li, Z., Hyseni, X., Carter, J. D., Soukup, J. M., Dailey, L. A., & Huang, Y.-C. (2006). Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol, 291(2), C357–C365. https://doi.org/10.1152/ajpcell.00365.2005
Li, Zhuowei, Xhevahire Hyseni, Jacqueline D. Carter, Joleen M. Soukup, Lisa A. Dailey, and Yuh-Chin T. Huang. “Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells.Am J Physiol Cell Physiol 291, no. 2 (August 2006): C357–65. https://doi.org/10.1152/ajpcell.00365.2005.
Li Z, Hyseni X, Carter JD, Soukup JM, Dailey LA, Huang Y-CT. Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol. 2006 Aug;291(2):C357–65.
Li, Zhuowei, et al. “Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells.Am J Physiol Cell Physiol, vol. 291, no. 2, Aug. 2006, pp. C357–65. Pubmed, doi:10.1152/ajpcell.00365.2005.
Li Z, Hyseni X, Carter JD, Soukup JM, Dailey LA, Huang Y-CT. Pollutant particles enhanced H2O2 production from NAD(P)H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol. 2006 Aug;291(2):C357–C365.

Published In

Am J Physiol Cell Physiol

DOI

ISSN

0363-6143

Publication Date

August 2006

Volume

291

Issue

2

Start / End Page

C357 / C365

Location

United States

Related Subject Headings

  • Rats, Sprague-Dawley
  • Rats
  • Rabbits
  • Pulmonary Artery
  • Physiology
  • Particle Size
  • Oxidative Stress
  • NADP
  • Mitochondria
  • In Vitro Techniques