title: Tissue factor and monocyte chemoattractant protein-1 expression in hypertensive individuals with normal or increased carotid intima-media wall thickness.
abstract: BACKGROUND
  People with hypertension display an inflammatory pattern that includes increased plasma concentrations of monocyte chemoattractant protein 1 (MCP-1) and C-reactive protein (CRP) and enhanced expression of tissue factor (TF) mRNA in blood monocytes.
  
  
  METHODS
  In this study, we investigated the relationship between CRP concentrations and TF and MCP-1 mRNA expression in unstimulated and lipopolysaccharide (LPS)-stimulated monocytes isolated from hypertensives with or without an increase in carotid intima-media thickness (IMT). We also investigated the expression of TF and MCP-1 mRNA and MCP-1 protein after in vitro addition of CRP to monocytes. We measured CRP (by immunonephelometry) and monocyte expression of TF and MCP-1 (by real-time PCR) in 80 untreated hypertensive patients without clinical cardiovascular disease (CVD) or additional risk factors for CVD compared with 41 controls. Based on IMT measured by carotid Doppler ultrasonography, patients were classified into the categories of normal (< or =1 mm) or abnormal (>1 mm). TF and MCP-1 mRNA and MCP-1 protein (by Western blotting) were measured after in vitro addition of CRP to monocytes from 10 randomized controls as well as 10 hypertensives with IMT < or =1 mm and 10 with IMT >1 mm.
  
  
  RESULTS
  CRP and TF and MCP-1 mRNA concentrations were significantly higher in IMT >1 mm hypertensives vs those with IMT < or =1 mm and controls. CRP had no effect on monocyte TF mRNA from either hypertensives or controls. CRP-stimulated monocytes from hypertensives, however, showed increased MCP-1 mRNA and protein expression compared with controls and LPS-stimulated cells.
  
  
  CONCLUSIONS
  Our findings suggest that the inflammatory response of blood monocytes plays an important role in the development of atherosclerosis and hypertension.
authors.affiliation: Department of Internal Medicine, University of Messina, Messina, Italy.
authors.forename: Maria A
authors.initials: MA
authors.lastname: Sardo
authors.forename: Salvatore
authors.initials: S
authors.lastname: Campo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mandraffino
authors.forename: Carlo
authors.initials: C
authors.lastname: Saitta
authors.forename: Antonio
authors.initials: A
authors.lastname: Bonaiuto
authors.forename: Maria
authors.initials: M
authors.lastname: Castaldo
authors.forename: Maurizio
authors.initials: M
authors.lastname: Cinquegrani
authors.forename: Giovanni
authors.initials: G
authors.lastname: Pizzimenti
authors.forename: Antonino
authors.initials: A
authors.lastname: Saitta
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000473:pathology*; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000473:pathology; D002343:Carotid Artery, Internal / Q000000981:diagnostic imaging / Q000473:pathology; D016893:Carotid Stenosis / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D013925:Thromboplastin / Q000096:biosynthesis* / Q000235:genetics; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology*; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology*; D014463:Ultrasonography
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D008070:Lipopolysaccharides; D002097:C-Reactive Protein; D013925:Thromboplastin