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Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor.

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Date
2005-08
Authors
Li, Zhuowei
Carter, Jacqueline D
Dailey, Lisa A
Huang, Yuh-Chin T
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Abstract
Exposure to particulate matter (PM) is associated with acute cardiovascular mortality and morbidity, but the mechanisms are not entirely clear. In this study, we hypothesized that PM may activate the angiotensin type 1 receptor (AT1R), a G protein-coupled receptor that regulates inflammation and vascular function. We investigated the acute effects of St. Louis, Missouri, urban particles (UPs; Standard Reference Material 1648) on the constriction of isolated rat pulmonary artery rings and the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 mitogen-activated protein kinases (MAPKs) in human pulmonary artery endothelial cells with or without losartan, an antagonist of AT1R. UPs at 1-100 microg/mL induced acute vasoconstriction in pulmonary artery. UPs also produced a time- and dose-dependent increase in phosphorylation of ERK1/2 and p38 MAPK. Losartan pretreatment inhibited both the vasoconstriction and the activation of ERK1/2 and p38. The water-soluble fraction of UPs was sufficient for inducing ERK1/2 and p38 phosphorylation, which was also losartan inhibitable. Copper and vanadium, two soluble transition metals contained in UPs, induced pulmonary vasoconstriction and phosphorylation of ERK1/2 and p38, but only the phosphorylation of p38 was inhibited by losartan. The UP-induced activation of ERK1/2 and p38 was attenuated by captopril, an angiotensin-converting enzyme inhibitor. These results indicate that activation of the local renin-angiotensin system may play an important role in cardiovascular effects induced by PM.
Type
Journal article
Subject
Pulmonary Artery
Cells, Cultured
Endothelial Cells
Animals
Humans
Rats
Rats, Sprague-Dawley
Copper
Vanadium
Losartan
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
p38 Mitogen-Activated Protein Kinases
Receptor, Angiotensin, Type 1
Dust
Air Pollutants
Cities
Air Pollution
Phosphorylation
Vasoconstriction
Particle Size
Missouri
In Vitro Techniques
Permalink
https://hdl.handle.net/10161/22251
Published Version (Please cite this version)
10.1289/ehp.7736
Publication Info
Li, Zhuowei; Carter, Jacqueline D; Dailey, Lisa A; & Huang, Yuh-Chin T (2005). Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor. Environmental health perspectives, 113(8). pp. 1009-1014. 10.1289/ehp.7736. Retrieved from https://hdl.handle.net/10161/22251.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Huang

Yuh-Chin Tony Huang

Professor of Medicine
Closed loop ventilation Environmental medicine Oxidative lung injuryCOPDHyperpolarized 129Xe MRI and regional lung function
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