title: Atorvastatin modifies the protein profile of circulating human monocytes after an acute coronary syndrome.
abstract: Aggressive treatment with high-dose atorvastatin reduces more effectively the incidence of cardiovascular events than moderate statin therapy. The mechanism of this benefit has not been fully elucidated. In order to know the potential effects of statin treatment on the protein expression of circulating monocytes in acute coronary syndrome (ACS) patients, a proteomic analysis of these cells was carried out by 2-DE and MS. Twenty-five patients with non-ST-elevation acute coronary syndrome (NSTEACS) were randomized, the fourth day after admission, to receive ATV 80 mg/dL (n = 14) or conventional treatment (CT) (n = 11), for two months. Blood was withdrawn at the end of the treatment, and monocytes were extracted for proteomic analysis and their protein expression patterns determined. Age, sex, total cholesterol, LDL, HDL, triglycerides, body mass index, presence of hypertension, diabetes, and smoking status were not significantly different between the two groups of patients. The expression of 20 proteins was modified by intensive ATV. Among the most relevant results stand out the normalization by intensive ATV treatment of the expression of proteins that modulate inflammation and thrombosis such as protein disulfide isomerase ER60 (PDI), Annexin I, and prohibitin, or that have other protective effects as HSP-70. Thus, this approach shed light at the molecular level of the beneficial mechanisms of anti-atherothrombotic drugs.
authors.affiliation: Department of Immunology, Fundación Jiménez Díaz, Madrid, Spain.
authors.forename: María G
authors.initials: MG
authors.lastname: Barderas
authors.forename: José
authors.initials: J
authors.lastname: Tuñón
authors.forename: Verónica M
authors.initials: VM
authors.lastname: Dardé
authors.forename: Fernando
authors.initials: F
authors.lastname: De la Cuesta
authors.forename: José J
authors.initials: JJ
authors.lastname: Jiménez-Nácher
authors.forename: Nieves
authors.initials: N
authors.lastname: Tarín
authors.forename: Lorenzo
authors.initials: L
authors.lastname: López-Bescós
authors.forename: Jesús
authors.initials: J
authors.lastname: Egido
authors.forename: Fernando
authors.initials: F
authors.lastname: Vivanco
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy / Q000378:metabolism*; D000368:Aged; D000924:Anticholesteremic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000069059:Atorvastatin; D016009:Chi-Square Distribution; D004305:Dose-Response Relationship, Drug; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D020869:Gene Expression Profiling; D006360:Heat-Shock Proteins / Q000378:metabolism; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use; D018709:Statistics, Nonparametric; D053719:Tandem Mass Spectrometry; D013927:Thrombosis / Q000378:metabolism
chemical_list: D000924:Anticholesteremic Agents; D006360:Heat-Shock Proteins; D006538:Heptanoic Acids; D008055:Lipids; D011758:Pyrroles; D000069059:Atorvastatin