title: Persistent and selective upregulation of renin-angiotensin system in circulating T lymphocytes in unstable angina.
abstract: BACKGROUND
  Unstable angina is associated with an acute systemic inflammatory reaction and circulating T lymphocytes are activated. We investigated whether in unstable angina with marked immune system activation a selective upregulation of the circulating T-cell renin-angiotensin system, modulated by angiotensin II, could occur.
  
  
  METHODS
  We studied 13 unstable angina patients, 10 patients with stable angina and 10 healthy subjects. After T-lymphocyte isolation, mRNAs for angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor (AT1-R) were quantified at baseline and after angiotensin II stimulation. ACE activity in cell pellet and supernatant and angiotensin II cell content were measured.
  
  
  RESULTS
  Plasma renin activity was similar in controls, stable and unstable angina patients. At baseline ACE and AT1-R mRNA levels were higher ( P<0.05) in T cells from unstable angina patients than in T cells from stable angina patients and controls, and further increased after angiotensin II addition to cultured T cells. ACE activity of unstable angina T cells was significantly higher than that of T cells from controls and stable angina patients. Only in T cells from unstable angina patients did angiotensin II stimulation cause the almost complete release of ACE activity in the supernatant.
  
  
  CONCLUSIONS
  The circulating T-cell-based renin-angiotensin system from unstable angina patients was selectively upregulated. In vivo unstable angina T cells could locally increase angiotensin II concentration in tissues where they migrate independently of the circulating renin-angiotensin system.
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy.
authors.forename: Mirella
authors.initials: M
authors.lastname: Coppo
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy.
authors.forename: Manuela
authors.initials: M
authors.lastname: Bandinelli
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Chiostri
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy.
authors.forename: Loredana
authors.initials: L
authors.lastname: Poggesi
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy.
authors.forename: Maria
authors.initials: M
authors.lastname: Boddi
mesh_terms: D000789:Angina, Unstable / Q000097:blood / Q000235:genetics / Q000276:immunology*; D000804:Angiotensin II / Q000494:pharmacology; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics / Q000378:metabolism; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000235:genetics; D013601:T-Lymphocytes / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D007371:Interferon-gamma; D002097:C-Reactive Protein; D007703:Peptidyl-Dipeptidase A; D012083:Renin
keywords: Angiotensin-converting enzyme; T cell; angiotensin II; renin–angiotensin system; unstable angina