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

doi:10.1186/s12940-017-0292-7

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 journal › Article › Academic › peer-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 language	English
Article number	87
Number of pages	15
Journal	Environmental Health
Volume	16
DOIs	https://doi.org/10.1186/s12940-017-0292-7
Publication status	Published - 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

Access to Document

10.1186/s12940-017-0292-7Licence: CC BY

Cite this

Winckelmans, E., Nawrot, T. S., Tsamou, M., Den Hond, E., Baeyens, W., Kleinjans, J., Lefebvre, W., Van Larebeke, N., Peusens, M., Plusquin, M., Reynders, H., Schoeters, G., Vanpoucke, C., de Kok, T. M., & Vrijens, K. (2017). Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure. Environmental Health, 16, Article 87. https://doi.org/10.1186/s12940-017-0292-7

@article{69313513a67a471989aeaeb4d9d243e4,

title = "Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure",

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-valueConclusions: 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.",

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

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

year = "2017",

month = aug,

day = "18",

doi = "10.1186/s12940-017-0292-7",

language = "English",

volume = "16",

journal = "Environmental Health",

issn = "1476-069X",

publisher = "BioMed Central Ltd",

}

Winckelmans, E, Nawrot, TS, Tsamou, M, Den Hond, E, Baeyens, W, Kleinjans, J, Lefebvre, W, Van Larebeke, N, Peusens, M, Plusquin, M, Reynders, H, Schoeters, G, Vanpoucke, C, de Kok, TM & Vrijens, K 2017, 'Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure', Environmental Health, vol. 16, 87. https://doi.org/10.1186/s12940-017-0292-7

TY - JOUR

T1 - Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure

AU - Winckelmans, Ellen

AU - Nawrot, Tim S.

AU - Tsamou, Maria

AU - Den Hond, Elly

AU - Baeyens, Willy

AU - Kleinjans, Jos

AU - Lefebvre, Wouter

AU - Van Larebeke, Nicolas

AU - Peusens, Martien

AU - Plusquin, Michelle

AU - Reynders, Hans

AU - Schoeters, Greet

AU - Vanpoucke, Charlotte

AU - de Kok, Theo M.

AU - Vrijens, Karen

PY - 2017/8/18

Y1 - 2017/8/18

N2 - 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-valueConclusions: 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.

AB - 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-valueConclusions: 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.

KW - Ambient air pollution

KW - Particulate matter

KW - Transcriptome-wide analyses

KW - Sex-specific

KW - mitochondria

KW - OXIDATIVE STRESS

KW - DISPERSION MODELS

KW - DAMAGE

KW - DYSFUNCTION

KW - APOPTOSIS

KW - PRESSURE

KW - EXERCISE

KW - SMOKERS

KW - HEALTH

KW - CANCER

U2 - 10.1186/s12940-017-0292-7

DO - 10.1186/s12940-017-0292-7

M3 - Article

C2 - 28821289

SN - 1476-069X

VL - 16

JO - Environmental Health

JF - Environmental Health

M1 - 87

ER -