TY - JOUR
T1 - Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases
AU - Chatziioannou, Aristotelis
AU - Georgiadis, Panagiotis
AU - Hebels, Dennie G.
AU - Liampa, Irene
AU - Valavanis, Ioannis
AU - Bergdahl, Ingvar A.
AU - Johansson, Anders
AU - Palli, Domenico
AU - Chadeau-Hyam, Marc
AU - Siskos, Alexandros P.
AU - Keun, Hector
AU - Botsivali, Maria
AU - de Kok, Theo M. C. M.
AU - Perez, Almudena Espin
AU - Kleinjans, Jos C. S.
AU - Vineis, Paolo
AU - Kyrtopoulos, Soterios A.
AU - EnviroGenomarkers Project Consorti
PY - 2017/2/22
Y1 - 2017/2/22
N2 - 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.
AB - 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.
KW - OBSTRUCTIVE PULMONARY-DISEASE
KW - CORONARY-HEART-DISEASE
KW - SEX-DIFFERENCES
KW - LUNG-CANCER
KW - PLATELET ACTIVATION
KW - GENE-EXPRESSION
KW - MYOCARDIAL-INFARCTION
KW - CIGARETTE-SMOKING
KW - HEME OXYGENASE-1
KW - RISK-FACTOR
U2 - 10.1038/srep42870
DO - 10.1038/srep42870
M3 - Article
C2 - 28225026
SN - 2045-2322
VL - 7
JO - Scientific Reports
JF - Scientific Reports
M1 - 42870
ER -