Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases
Journal
Scientific Reports
Journal Volume
7
Journal Issue
1
Date Issued
2017-02-22
Author(s)
Chatziioannou, Aristotelis
Georgiadis, Panagiotis
Hebels, Dennie G.
Liampa, Irene
Valavanis, Ioannis
Bergdahl, Ingvar A.
Johansson, Anders
Palli, Domenico
Chadeau-Hyam, Marc
Siskos, Alexandros P.
Keun, Hector
Botsivali, Maria
De Kok, Theo M.C.M.
Pérez, Almudena Espín
Kleinjans, Jos C.S.
Vineis, Paolo
Kyrtopoulos, Soterios A.
Gottschalk, Ralph
Van Leeuwen, Danitsja
Timmermans, Leen
Bendinelli, Benedetta
Kelly, Rachel
Vermeulen, Roel
Portengen, Lutzen
Saberi-Hosnijeh, Fatemeh
Melin, Beatrice
Hallmans, Goran
Lenner, Per
Athersuch, Toby J.
Kogevinas, Manolis
Stephanou, Euripides G.
Myridakis, Antonis
Fazzo, Lucia
De Santis, Marco
Comba, Pietro
Kiviranta, Hannu
Rantakokko, Panu
Airaksinen, Riikka
Ruokojarvi, Paivi
Gilthorpe, Mark
Fleming, Sarah
Fleming, Thomas
Jonsson, Bo
Lundh, Thomas
Liao, Shu Fen
Abstract
We recently reported that differential gene expression and DNA methylation profiles in blood leukocytes of apparently healthy smokers predicts with remarkable efficiency diseases and conditions known to be causally associated with smoking, suggesting that blood-based omic profiling of human populations may be useful for linking environmental exposures to potential health effects. Here we report on the sex-specific effects of tobacco smoking on transcriptomic and epigenetic features derived from genome-wide profiling in white blood cells, identifying 26 expression probes and 92 CpG sites, almost all of which are affected only in female smokers. Strikingly, these features relate to numerous genes with a key role in the pathogenesis of cardiovascular disease, especially thrombin signaling, including the thrombin receptors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5 (glycoprotein 5), as well as HMOX1 (haem oxygenase 1) and BCL2L1 (BCL2-like 1) which are involved in protection against oxidative stress and apoptosis, respectively. These results are in concordance with epidemiological evidence of higher female susceptibility to tobacco-induced cardiovascular disease and underline the potential of blood-based omic profiling in hazard and risk assessment.
Subjects
SEX-DIFFERENCES; LUNG-CANCER; GENE-EXPRESSION; CIGARETTE-SMOKING; HEME OXYGENASE-1; RISK-FACTOR; PLATELET; WOMEN; MEN; METAANALYSIS
Publisher
NATURE PUBLISHING GROUP
Type
journal article