Linked Life Data

19251948

Source:http://linkedlifedata.com/resource/pubmed/id/19251948

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-10-21
pubmed:abstractText
Exposure to pollutant particles increased respiratory morbidity and mortality. The alveolar macrophages (AMs) are one cell type in the lung directly exposed to particles. Upon contact with particles, AMs are activated and produce reactive oxygen species, but the scope of this oxidative stress response remains poorly defined. In this study, we determined the gene expression profile in human AMs exposed to particles, and sought to characterize the global response of pro- and antioxidant genes. We exposed AMs obtained by bronchoscopy from normal individuals to Chapel Hill particulate matter of 2.5-microm diameter or smaller (PM(2.5); 1 microg/ml) or vehicle for 4 hours (n = 6 independent samples). mRNAs were extracted, amplified, and hybridized to Agilent human 1A microarray. Significant genes were identified by significance analysis of microarrays (false discovery rate, 10%; P < or = 0.05) and mapped with Gene Ontology in the Database for Annotation, Visualization, and Integrated Discovery. We found 34 and 41 up- and down-regulated genes, respectively; 22 genes (approximately 30%) were involved in metal binding, and 11 were linked to oxidative stress, including up-regulation of five metallothionein (MT)-1 isoforms. Exogenous MT1 attenuated PM(2.5)-induced H2O2 release. PM(2.5) premixed with MT1 stimulated less H2O2 release. Knockdown of MT1F gene increased PM(2.5)-induced H2O2 release. PM(2.5) at 1 microg/ml did not increase H2O2 release. Mount St. Helens PM(2.5) and acid-extracted Chapel Hill PM(2.5), both poor in metals, did not induce MT1F or H2O2 release. Our results show that PM(2.5) induced a gene expression profile prevalent with genes related to metal binding and oxidative stress in human AMs, independent of oxidative stress. Metals associated with PM may play an important role in particle-induced gene changes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1535-4989
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
544-52
pubmed:dateRevised
2010-11-2
pubmed:meshHeading
pubmed-meshheading:19251948-Air Pollutants, pubmed-meshheading:19251948-Bronchoscopy, pubmed-meshheading:19251948-Cells, Cultured, pubmed-meshheading:19251948-Cluster Analysis, pubmed-meshheading:19251948-Databases, Genetic, pubmed-meshheading:19251948-Dose-Response Relationship, Drug, pubmed-meshheading:19251948-Gene Expression Profiling, pubmed-meshheading:19251948-Gene Expression Regulation, Enzymologic, pubmed-meshheading:19251948-Humans, pubmed-meshheading:19251948-Hydrogen Peroxide, pubmed-meshheading:19251948-Macrophage Activation, pubmed-meshheading:19251948-Macrophages, Alveolar, pubmed-meshheading:19251948-Metallothionein, pubmed-meshheading:19251948-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:19251948-Oxidative Stress, pubmed-meshheading:19251948-Particle Size, pubmed-meshheading:19251948-Particulate Matter, pubmed-meshheading:19251948-Polymerase Chain Reaction, pubmed-meshheading:19251948-RNA Interference, pubmed-meshheading:19251948-Up-Regulation
pubmed:year
2009
pubmed:articleTitle
Fine ambient particles induce oxidative stress and metal binding genes in human alveolar macrophages.
pubmed:affiliation
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27705, USA. huang002@mc.duke.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Intramural