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Regulating role of fetal thyroid hormones on placental mitochondrial DNA methylation: epidemiological evidence from the ENVIRONAGE birth cohort study

Overview of attention for article published in Clinical Epigenetics, June 2017
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Title
Regulating role of fetal thyroid hormones on placental mitochondrial DNA methylation: epidemiological evidence from the ENVIRONAGE birth cohort study
Published in
Clinical Epigenetics, June 2017
DOI 10.1186/s13148-017-0366-y
Pubmed ID
Authors

Bram G. Janssen, Hyang-Min Byun, Harry A. Roels, Wilfried Gyselaers, Joris Penders, Andrea A. Baccarelli, Tim S. Nawrot

Abstract

Fetal development largely depends on thyroid hormone availability and proper placental function with an important role played by placental mitochondria. The biological mechanisms by which thyroid hormones exert their effects on mitochondrial function are not well understood. We investigated the role of fetal thyroid hormones on placental mitochondrial DNA (mtDNA) content and mtDNA methylation. We collected placental tissue and cord blood from 305 mother-child pairs that were enrolled between February 2010 and June 2014 in the ENVIRONAGE (ENVIRonmental influence ON early AGEing) birth cohort (province of Limburg, Belgium). Placental mtDNA content was determined by qPCR and placental mtDNA methylation by bisulfite-pyrosequencing in two regions, i.e., the D-loop control region and 12S ribosomal RNA (MT-RNR1). The levels of free thyroid hormones (FT3, FT4) and thyroid-stimulating hormone (TSH) were measured in cord blood. Cord blood FT3 and FT4 were inversely associated with placental mtDNA methylation at the MT-RNR1 (p ≤ 0.01) and D-loop (p ≤ 0.05) regions, whereas a positive association was observed for both hormones with placental mtDNA content (p ≤ 0.04). Assuming causality, we estimated that MT-RNR1 and D-loop methylation mediated, respectively, 77% [indirect effect +14.61% (95% CI 2.64 to 27.98%, p = 0.01)] and 47% [indirect effect +8.60% (95% CI 1.23 to 16.50%, p = 0.02] of the positive association between FT3 and placental mtDNA content. Mediation models with FT4 gave similar results but the estimated effect proportions were smaller compared with those of FT3 (54% and 24%, respectively). We showed that epigenetic modification at specific loci of the mitochondrial genome could intervene with the thyroid-dependent regulation of mitochondrial DNA copy numbers.

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Mendeley readers

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The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 42 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 17%
Student > Master 5 12%
Professor 4 10%
Researcher 4 10%
Other 3 7%
Other 7 17%
Unknown 12 29%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 8 19%
Medicine and Dentistry 7 17%
Agricultural and Biological Sciences 4 10%
Nursing and Health Professions 2 5%
Neuroscience 2 5%
Other 5 12%
Unknown 14 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 30 June 2017.
All research outputs
#20,431,953
of 22,985,065 outputs
Outputs from Clinical Epigenetics
#1,119
of 1,262 outputs
Outputs of similar age
#275,951
of 316,862 outputs
Outputs of similar age from Clinical Epigenetics
#25
of 29 outputs
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