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

Content Provider	Springer Nature : BioMed Central
Author	Winckelmans, Ellen Nawrot, Tim S Tsamou, Maria Den Hond, Elly Baeyens, Willy Kleinjans, Jos Lefebvre, Wouter Van Larebeke, Nicolas Peusens, Martien Plusquin, Michelle Reynders, Hans Schoeters, Greet Vanpoucke, Charlotte de Kok, Theo M Vrijens, Karen
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 <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. 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.
Related Links	https://ehjournal.biomedcentral.com/counter/pdf/10.1186/s12940-017-0292-7.pdf
Ending Page	15
Page Count	15
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s12940-017-0292-7
Journal	Environmental Health
Issue Number	1
Volume Number	16
Language	English
Publisher	BioMed Central
Publisher Date	2017-08-18
Access Restriction	Open
Subject Keyword	Occupational Medicine Industrial Medicine Public Health Environmental Health Ambient air pollution Particulate matter Transcriptome-wide analyses Sex-specific mitochondria Occupational Medicine/Industrial Medicine
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Public Health, Environmental and Occupational Health
Journal Impact Factor	5.4/2023
5-Year Journal Impact Factor	6.7/2023

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