Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure

Environmental Health

Research

Charlotte Vanpoucke¹  Ellen Winckelmans²  Michelle Plusquin²  Karen Vrijens²  Martien Peusens²  Maria Tsamou²  Tim S Nawrot³  Willy Baeyens⁴  Nicolas Van Larebeke⁵  Jos Kleinjans⁶  Theo M de Kok⁶  Hans Reynders⁷  Wouter Lefebvre⁸  Greet Schoeters⁹  Elly Den Hond^1,10 

[1] Belgian Interregional Environment Agency (IRCEL), Brussels, Belgium;Centre for Environmental Sciences, Hasselt University, Agoralaan gebouw D, B-3590, Diepenbeek, Belgium;Centre for Environmental Sciences, Hasselt University, Agoralaan gebouw D, B-3590, Diepenbeek, Belgium;Department of Public Health & Primary Care, Leuven University, Leuven, Belgium;Department of Analytical and Environmental Chemistry, Vrije Universiteit Brussel, Brussels, Belgium;Department of Radiotherapy and Nuclear Medicine, Ghent University, Ghent, Belgium;Department of Toxicogenomics, Maastricht University, Maastricht, The Netherlands;Environment, Nature and Energy Department, Flemish Government, Brussels, Belgium;Flemish Institute for Technological Research, Mol, Belgium;Flemish Institute for Technological Research, Mol, Belgium;Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium;Institute of Public Health, Department of Environmental Medicine, University of Southern Denmark, Odense, Denmark;Provincial Institute for Hygiene, Antwerp, Belgium;

关键词: Ambient air pollution;    Particulate matter;    Transcriptome-wide analyses;    Sex-specific, mitochondria;   

DOI  :  10.1186/s12940-017-0292-7

 received in 2016-12-23, accepted in 2017-07-26,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundDue to their lack of repair capacity mitochondria are critical targets for environmental toxicants. We studied genes and pathways reflecting mitochondrial responses to short- and medium-term PM10 exposure.MethodsWhole genome gene expression was measured in peripheral blood of 98 adults (49% women). We performed linear regression analyses stratified by sex and adjusted for individual and temporal characteristics to investigate alterations in gene expression induced by short-term (week before blood sampling) and medium-term (month before blood sampling) PM10 exposure. Overrepresentation analyses (ConsensusPathDB) were performed to identify enriched mitochondrial associated pathways and gene ontology sets. Thirteen Human MitoCarta genes were measured by means of quantitative real-time polymerase chain reaction (qPCR) along with mitochondrial DNA (mtDNA) content in an independent validation cohort (n = 169, 55.6% women).ResultsOverrepresentation analyses revealed significant pathways (p-value <0.05) related to mitochondrial genome maintenance and apoptosis for short-term exposure and to the electron transport chain (ETC) for medium-term exposure in women. For men, medium-term PM10 exposure was associated with the Tri Carbonic Acid cycle. In an independent study population, we validated several ETC genes, including UQCRH and COX7C (q-value <0.05), and some genes crucial for the maintenance of the mitochondrial genome, including LONP1 (q-value: 0.07) and POLG (q-value: 0.04) in women.ConclusionsIn this exploratory study, we identified mitochondrial genes and pathways associated with particulate air pollution indicating upregulation of energy producing pathways as a potential mechanism to compensate for PM-induced mitochondrial damage.

【 授权许可】

CC BY   
© The Author(s). 2017