title: Nocturnal hypoxic stress activates invasive ability of monocytes in patients with obstructive sleep apnoea syndrome.
abstract: OBJECTIVE
  Obstructive sleep apnoea syndrome (OSAS) is known to be a risk factor for cardiovascular events. However, the precise mechanism has not been fully elucidated. OSAS-induced hypoxic stress may promote the production of inflammatory cytokines and chemokines by monocytes, which has a crucial role in the development of atherosclerosis. In addition, adhesion to the vascular endothelium and transendothelial migration of monocytes are considered to induce atherosclerosis. The aim of this study was to investigate the effects of hypoxic stress on the invasive ability of monocytes in OSAS.
  
  
  METHODS
  Twenty-one male patients with OSAS and 17 healthy male control subjects, who were matched for age and BMI, were enrolled. Venous blood samples were collected before and after sleep, and also after CPAP titration, for the purpose of monocyte isolation. The invasive ability of monocytes was evaluated by counting the number of invading cells using a BD BioCoat Matrigel Invasion Chamber.
  
  
  RESULTS
  The number of cells, which represents the invasive ability of monocytes, was significantly higher in patients with OSAS compared with control subjects, in the early morning (P < 0.001). In patients with OSAS, invasive ability in the early morning after sleep was significantly elevated as compared with that before sleep (P < 0.001), and was positively correlated with the oxygen desaturation index (P < 0.05). CPAP titration led to a decrease in the invasive ability (P < 0.001).
  
  
  CONCLUSIONS
  These results indicate that OSAS-induced hypoxic stress activates the invasive ability of monocytes, and that the occurrence of this phenomenon during sleep may contribute to the development of atherosclerosis in OSAS.
authors.affiliation: Second Department of Internal Medicine, Nara Medical University, Nara 634-8522, Japan.
authors.forename: Shinji
authors.initials: S
authors.lastname: Tamaki
authors.forename: Motoo
authors.initials: M
authors.lastname: Yamauchi
authors.forename: Atsuhiko
authors.initials: A
authors.lastname: Fukuoka
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Makinodan
authors.forename: Noriko
authors.initials: N
authors.lastname: Koyama
authors.forename: Koichi
authors.initials: K
authors.lastname: Tomoda
authors.forename: Masanori
authors.initials: M
authors.lastname: Yoshikawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kimura
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000453:epidemiology / Q000503:physiopathology; D016022:Case-Control Studies; D002452:Cell Count; D002465:Cell Movement / Q000502:physiology*; D002940:Circadian Rhythm / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000473:pathology*; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000473:pathology* / Q000503:physiopathology*