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Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases

Chatziioannou, Aristotelis; Georgiadis, Panagiotis; Hebels, Dennie G.; Liampa, Irene; Valavanis, Ioannis; Bergdahl, Ingvar A. LU ; Johansson, Anders; Palli, Domenico; Chadeau-Hyam, Marc and Siskos, Alexandros P., et al. (2017) In Scientific Reports 7.
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... (More)

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.

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Scientific Reports
volume
7
publisher
Nature Publishing Group
external identifiers
  • scopus:85013857766
ISSN
2045-2322
DOI
10.1038/srep42870
language
English
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yes
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917acb58-71f7-4fa3-aa3a-2651bf57cb1a
date added to LUP
2017-03-08 10:20:16
date last changed
2017-06-21 13:41:34
@article{917acb58-71f7-4fa3-aa3a-2651bf57cb1a,
  abstract     = {<p>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.</p>},
  articleno    = {42870},
  author       = {Chatziioannou, Aristotelis and Georgiadis, Panagiotis and Hebels, Dennie G. and Liampa, Irene and Valavanis, Ioannis and Bergdahl, Ingvar A. and Johansson, Anders and Palli, Domenico and Chadeau-Hyam, Marc and Siskos, Alexandros P. and Keun, Hector and Botsivali, Maria and De Kok, Theo M C M and Pérez, Almudena Espín and Kleinjans, Jos C S and Vineis, Paolo and Kyrtopoulos, Soterios A. and Gottschalk, Ralph and Van Leeuwen, Danitsja and Timmermans, Leen and Bendinelli, Benedetta and Kelly, Rachel and Vermeulen, Roel and Portengen, Lutzen and Saberi Hosnijeh, Fatemeh and Melin, Beatrice and Hallmans, Goran and Lenner, Per and Athersuch, Toby J. and Kogevinas, Manolis and Stephanou, Euripides G. and Myridakis, Antonis and Fazzo, Lucia and De Santis, Marco and Comba, Pietro and Kiviranta, Hannu and Rantakokko, Panu and Airaksinen, Riikka and Ruokojarvi, Paivi and Gilthorpe, Mark and Fleming, Sarah and Fleming, Thomas and Tu, Yu Kang and Jönsson, Bo A and Lundh, Thomas and Chen, Wei-Jung and Lee, Wen Chung and Hsiao, Chuhsing Kate and Chien, Kuo Liong and Kuo, Po Hsiu and Hung, Hung and Liao, Shu Fen},
  issn         = {2045-2322},
  language     = {eng},
  month        = {02},
  publisher    = {Nature Publishing Group},
  series       = {Scientific Reports},
  title        = {Blood-based omic profiling supports female susceptibility to tobacco smoke-induced cardiovascular diseases},
  url          = {http://dx.doi.org/10.1038/srep42870},
  volume       = {7},
  year         = {2017},
}