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

Ellen Winckelmans, Tim S. Nawrot*, Maria Tsamou, Elly Den Hond, Willy Baeyens, Jos Kleinjans, Wouter Lefebvre, Nicolas Van Larebeke, Martien Peusens, Michelle Plusquin, Hans Reynders, Greet Schoeters, Charlotte Vanpoucke, Theo M. de Kok, Karen Vrijens

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background: Due 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.

Methods: Whole 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).

Results: Overrepresentation analyses revealed significant pathways (p-value

Conclusions: In 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.

Original languageEnglish
Article number87
Number of pages15
JournalEnvironmental Health
Volume16
DOIs
Publication statusPublished - 18 Aug 2017

Keywords

  • Ambient air pollution
  • Particulate matter
  • Transcriptome-wide analyses
  • Sex-specific
  • mitochondria
  • OXIDATIVE STRESS
  • DISPERSION MODELS
  • DAMAGE
  • DYSFUNCTION
  • APOPTOSIS
  • PRESSURE
  • EXERCISE
  • SMOKERS
  • HEALTH
  • CANCER

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