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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/19003

Title: Placental mitochondrial methylation and exposure to airborne particulate matter in the early life environment: An ENVIRONAGE birth cohort study
Authors: Janssen, Bram
Byun, Hyang-Min
Gyselaers, Wilfried
Lefebvre, Wouter
Baccarelli, Andrea A.
Nawrot, Tim
Issue Date: 2015
Citation: Epigenetics, 10 (6), p. 536-544
Abstract: Most research to date has focused on epigenetic modifications in the nuclear genome, with little attention devoted to mitochondrial DNA (mtDNA). Placental mtDNA content has been shown to respond to environmental exposures that induce oxidative stress, including airborne particulate matter (PM). Damaged or non-functioning mitochondria are specifically degraded through mitophagy, exemplified by lower mtDNA content, and could be primed by epigenetic modifications in the mtDNA. We studied placental mtDNA methylation in the context of the early life exposome. We investigated placental tissue from 381 mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mtDNA methylation by bisulfite-pyrosequencing in 2 regions, i.e., the D-loop control region and 12S rRNA (MT-RNR1), and measured mtDNA content by qPCR. PM2.5 exposure was calculated for each participant's home address using a dispersion model. An interquartile range (IQR) increment in PM2.5 exposure over the entire pregnancy was positively associated with mtDNA methylation (MT-RNR1: +0.91%, P = 0.01 and D-loop: +0.21%, P = 0.05) and inversely associated with mtDNA content (relative change of -15.60%, P = 0.001) in placental tissue. mtDNA methylation was estimated to mediate 54% [P = 0.01 (MT-RNR1)] and 27% [P = 0.06 (D-loop)] of the inverse association between PM2.5 exposure and mtDNA content. This study provides new insight into the mechanisms of altered mitochondrial function in the early life environment. Epigenetic modifications in the mitochondrial genome, especially in the MT-RNR1 region, substantially mediate the association between PM2.5 exposure during gestation and placental mtDNA content, which could reflect signs of mitophagy and mitochondrial death.
Notes: [Janssen, Bram G.; Nawrot, Tim S.] Hasselt Univ, Ctr Environm Sci, Diepenbeek, Belgium. [Byun, Hyang-Min; Baccarelli, Andrea A.] Harvard Univ, Sch Publ Hlth, Exposure Epidemiol & Risk Program, Lab Environm Epigenet, Boston, MA 02115 USA. [Gyselaers, Wilfried] East Limburg Hosp, Dept Obstet, Genk, Belgium. [Gyselaers, Wilfried] Hasselt Univ, Dept Physiol, Diepenbeek, Belgium. [Lefebvre, Wouter] Flemish Inst Technol Res VITO, Mol, Belgium. [Nawrot, Tim S.] Leuven Univ KU Leuven, Dept Publ Hlth Occupat Environm & Insurance Med, Leuven, Belgium.
URI: http://hdl.handle.net/1942/19003
DOI: 10.1080/15592294.2015.1048412
ISI #: 000355682500010
ISSN: 1559-2294
Category: A1
Type: Journal Contribution
Validation: ecoom, 2016
Appears in Collections: Research publications

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