title: Rosuvastatin may reduce the incidence of cardiovascular events in patients with acute coronary syndromes receiving percutaneous coronary intervention by suppressing miR-155/SHIP-1 signaling pathway.
abstract: OBJECTIVE
  The beneficial effect of rosuvastatin against percutaneous coronary intervention (PCI) related procedural myocardial injury has been determined mostly in patients with acute coronary syndromes (ACS). However, the detailed therapeutic mechanism has not been well studied.
  
  
  METHODS
  Patients with ACS receiving PCI (n = 159) were randomized to control group (placebo treatment) or to rosuvastatin group (20 mg 12 h before PCI, and a further 20 mg 2 h preprocedure dose). Levels of INF-γ, TNF-α, IL-6, miR-155/SHIP-1, and CD4(+)FoxP3(+)Treg in peripheral blood were detected before PCI and 24 h after PCI. Clinical data of these patients were also collected in this prospective study.
  
  
  RESULTS
  Compared with placebo, rosuvastatin treatment significantly reduced the incidence of periprocedural myocardial infarction (PMI) and levels of cardiac troponin I (cTnI) associated with decreased relative expression of serum miR-155, levels of inflammatory cytokines (INF-γ, TNF-α, and IL-6), increased SHIP-1 expression and CD4(+)FoxP3(+)Treg percentage values (P < 0.05). In addition, patients with rosuvastatin pretreatment also reduced incidence of 30 days major adverse cardiac events (MACE) compared to the patients with placebo treatment (16 patients vs. 28 patients, P = 0.038).
  
  
  CONCLUSIONS
  Our study suggests that high loading dose rosuvastatin pretreatment may reduce the incidence of cardiovascular events and levels of inflammatory markers in patients with ACS receiving PCI, which may be explained at least in part, by mechanism involving suppression of miR-155/SHIP-1 signaling pathway.
authors.affiliation: Department of Cardiology, Yulin First People's Hospital, Sixth Affiliated Hospital of Guangxi Medical University, Yulin, Guangxi, China.
authors.forename: Wenchao
authors.initials: W
authors.lastname: Xie
authors.forename: Ping
authors.initials: P
authors.lastname: Li
authors.forename: Zhengdong
authors.initials: Z
authors.lastname: Wang
authors.forename: Jian
authors.initials: J
authors.lastname: Chen
authors.forename: Zhihai
authors.initials: Z
authors.lastname: Lin
authors.forename: Xiangwen
authors.initials: X
authors.lastname: Liang
authors.forename: Yingxi
authors.initials: Y
authors.lastname: Mo
mesh_terms: D054058:Acute Coronary Syndrome / Q000628:therapy*; D000368:Aged; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D016207:Cytokines / Q000097:blood; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D000072181:Inositol Polyphosphate 5-Phosphatases; D008297:Male; D035683:MicroRNAs / Q000037:antagonists & inhibitors* / Q000502:physiology; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention; D000072183:Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases; D010744:Phosphoric Monoester Hydrolases / Q000037:antagonists & inhibitors* / Q000502:physiology; D011446:Prospective Studies; D011743:Pyrimidines / Q000627:therapeutic use*; D000068718:Rosuvastatin Calcium; D015398:Signal Transduction / Q000187:drug effects*; D013449:Sulfonamides / Q000627:therapeutic use*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
chemical_list: D016207:Cytokines; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium; D010744:Phosphoric Monoester Hydrolases; D000072181:Inositol Polyphosphate 5-Phosphatases; C000606430:INPP5D protein, human; D000072183:Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
keywords: Acute coronary syndromes; Percutaneous coronary intervention; Rosuvastatin; miR-155/SHIP-1