title: Pattern of expression of inflammatory markers in adipose tissue of untreated hypertensive patients.
abstract: OBJECTIVE
  Adiposity contributes to the insulin resistance and endothelial dysfunction of the hypertensive state; the inflammatory network and the metalloprotease (MMP)/ tissue inhibitor of metalloprotease (TIMP) system modulate vascular structure and function.
  
  
  METHODS
  We measured interleukin-6 (IL-6); plasminogen activator inhibitor-1 (PAI-1); tumor necrosis factor-alpha; transforming growth factor-beta; MMP-2, MMP-9, TIMP-1, and TIMP-2 expression; MMP-2 and MMP-9 activity; and TIMP-1 and TIMP-2 protein in adipocytes isolated from paired samples of visceral and subcutaneous adipose tissue of 30 nonobese, untreated hypertensive patients and 20 normotensive controls.
  
  
  RESULTS
  Although expression of IL-6, PAI-1, tumor necrosis factor-alpha, and transforming growth factor-beta were generally higher in visceral adipocytes, IL-6, PAI-1, and tumor necrosis factor-alpha were overexpressed, and transforming growth factor-beta was underexpressed in hypertensive vs. controls (all P<0.0001). These changes were paralleled by higher circulating IL-6 and PAI-1 levels in hypertensive patients. MMP-2 and TIMP-2 expression - which were higher in subcutaneous than visceral cells - were reduced in hypertensive patients (all P<0.0001), whereas MMP-9 and TIMP-1 did not differ between the two groups. Both MMP-2 and MMP-9 activity were reduced in hypertensive patients (all P<0.0001). In the whole dataset, SBP and DBP were directly related to IL-6 and PAI-1 expression and inversely to MMP-2 and MMP-9 activity.
  
  
  CONCLUSIONS
  Adipocytes from both visceral and subcutaneous depots of untreated hypertensive patients show a pattern of expression of inflammatory and MMP/TIMP molecules that is compatible with the raised circulating levels of inflammatory markers, is quantitatively related to the height of blood pressure, and provides the cellular basis for the proinflammatory and prothrombotic predisposition of these patients.
authors.affiliation: Department of Internal Medicine, University of Pisa, Pisa, Italy.
authors.forename: Stephanie
authors.initials: S
authors.lastname: Madec
authors.forename: Massimo
authors.initials: M
authors.lastname: Chiarugi
authors.forename: Eleonora
authors.initials: E
authors.lastname: Santini
authors.forename: Chiara
authors.initials: C
authors.lastname: Rossi
authors.forename: Paolo
authors.initials: P
authors.lastname: Miccoli
authors.forename: Ele
authors.initials: E
authors.lastname: Ferrannini
authors.forename: Anna
authors.initials: A
authors.lastname: Solini
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000368:Aged; D015415:Biomarkers / Q000032:analysis; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D020782:Matrix Metalloproteinases / Q000032:analysis / Q000378:metabolism; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis / Q000097:blood; D040521:Subcutaneous Tissue / Q000378:metabolism; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000032:analysis / Q000097:blood; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000032:analysis; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000378:metabolism / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D019715:Tissue Inhibitor of Metalloproteinase-1; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D019716:Tissue Inhibitor of Metalloproteinase-2; D020782:Matrix Metalloproteinases; D020780:Matrix Metalloproteinase 9