title: Downregulation of peroxisome proliferator-activated receptor-gamma expression in hypertensive atrial fibrillation.
abstract: BACKGROUND
  Numerous evidence has suggested that either hypertension or atrial fibrillation (AF) is associated with systemic inflammation. Peroxisome proliferator-activated receptor-gamma (PPARgamma) has been proved to have anti-inflammatory effects and is implicated as a molecular pathway involved in many cardiovascular diseases, such as hypertension. The correlation between PPARgamma inflammation and AF is still unknown.
  
  
  METHODS
  Using a case-control study design, 57 patients with hypertensive AF (persistent AF: 32, paroxysmal AF: 25) were included into the study groups. A total of 32 age-matched patients with hypertension, but without AF were selected as the control group. The expressions of PPARgamma, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) mRNA in monocytes were detected by using a reverse transcription-polymerase chain reaction (RT-PCR). Interleukin-1 (IL-1) was measured by immunoenzymetric methods.
  
  
  RESULTS
  The PPARgamma mRNA was markedly decreased in the hypertensive AF group as compared with the hypertensive non-AF group, and it was significantly lower in persistent AF than paroxysmal AF (0.222 +/- 0.0702 vs 0.564 +/- 0.0436, P<0.01). TNF-alpha mRNA, IL-6 mRNA, and IL-1 were increased in patients with hypertensive AF compared to the non-AF group and it was even higher in persistent AF than in paroxysmal AF (0.721 +/- 0.0541 vs 0.530 +/- 0.0496, 0.567 +/- 0.044 vs 0.457 +/- 0.0505, 325.61 +/- 88.10 vs 190.65 +/- 59.38, respectively, P<0.01). TNF-alpha, IL-6, and IL-1 were in negative correlation with PPARgamma, the correlation coefficient was -0.854, -0.769, and -0.702, respectively (P<0.01).
  
  
  CONCLUSIONS
  In hypertensive patients, increased inflammatory cytokines were associated with increased incidence of AF and atrial remodeling; PPARgamma may be involved in the pathogenesis of AF by regulation of inflammation.
authors: Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China. xiaopingchen0196@126.com
authors: Xiaoping
authors: X
authors: Chen
authors: Ziyi
authors: Z
authors: Bing
authors: Jiyun
authors: J
authors: He
authors: Lingyun
authors: L
authors: Jiang
authors: Xiaojia
authors: X
authors: Luo
authors: Yanling
authors: Y
authors: Su
authors: Bing
authors: B
authors: Kan
authors: Dejia
authors: D
authors: Huang
authors: Yuquan
authors: Y
authors: Wei
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D016022:Case-Control Studies; D015536:Down-Regulation; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000235:genetics / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000235:genetics; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D047495:PPAR gamma / Q000097:blood / Q000235:genetics*; D012333:RNA, Messenger / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: C508600:IL6 protein, human; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D047495:PPAR gamma; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha