| Iron chelation inhibits the development of pulmonary vascular remodeling. | |
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MedLine Citation:
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PMID: 22974762 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Reactive oxygen species (ROS) have been implicated in the pathogenesis of pulmonary hypertension. Because iron is an important regulator of ROS biology, this study examined the effects of iron chelation on the development of pulmonary vascular remodeling. The administration of an iron chelator, deferoxamine, to rats prevented chronic hypoxia-induced pulmonary hypertension and pulmonary vascular remodeling. Various iron chelators inhibited the growth of cultured pulmonary artery smooth muscle cells. Protein carbonylation, an important iron-dependent biological event, was promoted in association with pulmonary vascular remodeling and cell growth. A proteomic approach identified that Rho GDP-dissociation inhibitor (a negative regulator of RhoA) is carbonylated. In human plasma, the protein carbonyl content was significantly higher in patients with idiopathic pulmonary arterial hypertension than in healthy controls. These results suggest that iron plays an important role in the ROS-dependent mechanism underlying the development of pulmonary hypertension. |
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Authors:
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Chi-Ming Wong; Ioana R Preston; Nicholas S Hill; Yuichiro J Suzuki |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-08-25 |
Journal Detail:
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Title: Free radical biology & medicine Volume: 53 ISSN: 1873-4596 ISO Abbreviation: Free Radic. Biol. Med. Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-10-15 Completed Date: 2013-03-04 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 8709159 Medline TA: Free Radic Biol Med Country: United States |
Other Details:
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Languages: eng Pagination: 1738-47 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Proteins / metabolism Case-Control Studies Cell Proliferation / drug effects Cells, Cultured Deferoxamine / pharmacology*, therapeutic use Female Humans Hydralazine / pharmacology Hypertension, Pulmonary / blood, physiopathology, prevention & control Iron Chelating Agents / pharmacology*, therapeutic use Male Middle Aged Myocardial Contraction / drug effects Myocytes, Smooth Muscle / drug effects, metabolism Oxidation-Reduction Protein Carbonylation Pulmonary Artery / drug effects, pathology, physiopathology Rats Rats, Sprague-Dawley Reactive Oxygen Species / metabolism Vasodilator Agents / pharmacology rho Guanine Nucleotide Dissociation Inhibitor alpha / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL072844/HL/NHLBI NIH HHS; R01 HL097514/HL/NHLBI NIH HHS; R01HL72844/HL/NHLBI NIH HHS; R01HL97514/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Blood Proteins; 0/Iron Chelating Agents; 0/Reactive Oxygen Species; 0/Vasodilator Agents; 0/rho Guanine Nucleotide Dissociation Inhibitor alpha; 70-51-9/Deferoxamine; 86-54-4/Hydralazine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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