title: Increased levels of microparticles originating from endothelial cells, platelets and erythrocytes in subjects with metabolic syndrome: relationship with oxidative stress.
abstract: OBJECTIVE
  The Metabolic Syndrome (MetS) is associated with increased cardiovascular risk. Circulating microparticles (MP) are involved in the pathogenesis of atherothrombotic disorders and are raised in individual with CVD. We measured their level and cellular origin in subjects with MetS and analyzed their associations with 1/anthropometric and biological parameters of MetS, 2/inflammation and oxidative stress markers.
  
  
  RESULTS
  Eighty-eight subjects with the MetS according to the NCEP-ATPIII definition were enrolled in a bicentric study and compared to 27 healthy controls. AnnexinV-positive MP (TMP), MP derived from platelets (PMP), erythrocytes (ErMP), endothelial cells (EMP), leukocytes (LMP) and granulocytes (PNMP) were determined by flow cytometry. MetS subjects had significantly higher counts/μl of TMP (730.6±49.7 vs 352.8±35.6), PMP (416.0±43.8 vs 250.5±23.5), ErMP (243.8±22.1 vs 73.6±19.6) and EMP (7.8±0.8 vs 4.0±1.0) compared with controls. LMP and PNMP were not statistically different between groups. Multivariate analysis demonstrated that each criterion for the MetS influenced the number of TMP. Waist girth was a significant determinant of PMP and EMP level and blood pressure was correlated with EMP level. Glycemia positively correlated with PMP level whereas dyslipidemia influenced EMP and ErMP levels. Interestingly, the oxidative stress markers, plasma glutathione peroxydase and urinary 8-iso-prostaglandin F(2) α, independently influenced TMP and PMP levels whereas inflammatory markers did not, irrespective of MP type.
  
  
  CONCLUSIONS
  Increased levels of TMP, PMP, ErMP and EMP are associated with individual metabolic abnormalities of MetS and oxidative stress. Whether MP assessment may represent a marker for risk stratification or a target for pharmacological intervention deserves further investigation.
authors.affiliation: UMR INSERM 476, INRA 1260, Univ Aix-Marseille, Faculté de Médecine, 27 Boulevard Jean Moulin, Marseille Cedex 05, France.
authors.forename: O
authors.initials: O
authors.lastname: Helal
authors.forename: C
authors.initials: C
authors.lastname: Defoort
authors.forename: S
authors.initials: S
authors.lastname: Robert
authors.forename: C
authors.initials: C
authors.lastname: Marin
authors.forename: N
authors.initials: N
authors.lastname: Lesavre
authors.forename: J
authors.initials: J
authors.lastname: Lopez-Miranda
authors.forename: U
authors.initials: U
authors.lastname: Risérus
authors.forename: S
authors.initials: S
authors.lastname: Basu
authors.forename: J
authors.initials: J
authors.lastname: Lovegrove
authors.forename: J
authors.initials: J
authors.lastname: McMonagle
authors.forename: H M
authors.initials: HM
authors.lastname: Roche
authors.forename: F
authors.initials: F
authors.lastname: Dignat-George
authors.forename: D
authors.initials: D
authors.lastname: Lairon
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D055252:Cell-Derived Microparticles / Q000378:metabolism* / Q000473:pathology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D016014:Linear Models; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000473:pathology*; D008875:Middle Aged; D018384:Oxidative Stress; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1