title: Smoking and FOS expression from blood leukocyte transcripts in patients with coronary artery disease.
abstract: OBJECTIVE
  Analysis of the leukocyte transriptome, in particular the Finkel-Biskis-Jinkins Osteosarcoma (c-Fos) gene, which has a prominent role in inflammation, provides new insights into atherosclerosis mechanisms. Although smoking is a major risk factor, the links between smoking status and coronary artery disease (CAD) remains unclear. We aimed to analyze the relationship between smoking status and c-Fos expression in circulating leukocytes of patients with CAD.
  
  
  METHODS
  c-Fos expression was measured by RT-Q-PCR, from blood leukocytes of 239 consecutive patients after acute myocardial infarction (MI). The patients were asked about their smoking status and stratified into 3 groups: current smokers (CS) (N = 85), past smokers (PS) (N = 78) and never smokers (NS) (N = 76).
  
  
  RESULTS
  NS had a higher risk profile including hypertension, and CS were younger than PS and NS (-13 years and 17 years respectively). There was only a trend towards lower CRP levels in NS and PS than in CS. The mean c-Fos transcript level was slightly higher in CS than in PS and NS (0.924 vs. 0.908 and 0.861 AU, respectively; p = 0.005). By univariate analysis, neither age, nor sex, nor CRP nor white blood cell count was associated with c-Fos transcript levels. By multivariate analysis, CS (vs. PS + NS) was the strongest predictor of the c-Fos transcript level, (B = 0.042 ± 0.014, p = 0.003), even after adjustment for confounding factors (i.e. hypertension, chronic medication, family history of CAD, and prior MI).
  
  
  CONCLUSIONS
  Our work suggests that c-Fos transcript level in blood leukocyte could be considered a cumulative biomarker of smoking. As the c-Fos gene has been put forward as a new factor in the progression and severity of atherosclerosis, it could be considered a novel potential pathway of tobacco toxicity in coronary artery disease.
authors: IFR 100 Santé-STIC, Laboratoire de Physiopathologie et Pharmacologie Cardiovasculaires Expérimentales, UFR Médecine, Université de Bourgogne EA2979, Dijon, France.
authors: Sebastien
authors: S
authors: Saliques
authors: Jean-Raymond
authors: JR
authors: Teyssier
authors: Catherine
authors: C
authors: Vergely
authors: Luc
authors: L
authors: Lorgis
authors: Julie
authors: J
authors: Lorin
authors: Anne
authors: A
authors: Donzel
authors: Pierre
authors: P
authors: Sicard
authors: Juliane
authors: J
authors: Berchoud
authors: Sylviane
authors: S
authors: Ragot
authors: Claude
authors: C
authors: Touzery
authors: Yves
authors: Y
authors: Cottin
authors: Luc
authors: L
authors: Rochette
authors: Marianne
authors: M
authors: Zeller
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics*; D005260:Female; D005602:France; D016762:Genes, fos; D005819:Genetic Markers; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007962:Leukocytes / Q000378:metabolism*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics*; D011446:Prospective Studies; D012333:RNA, Messenger / Q000097:blood*; D018570:Risk Assessment; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D016540:Smoking Cessation; D000074606:Smoking Prevention
chemical_list: D005819:Genetic Markers; D018836:Inflammation Mediators; D012333:RNA, Messenger