title: Microparticles from Patients Undergoing Percutaneous Coronary Intervention Impair Vasodilatation by Uncoupling Endothelial Nitric Oxide Synthase.
abstract: Percutaneous coronary interventions (PCIs) save countless acute myocardial infarction (AMI) patients. However, endothelial injury is still an inevitable complication. Circulating microparticles (MPs) play important roles in vascular dysfunction. Whether PCI affects function of MPs remains unclear.
  
  
  
  MPs were obtained from AMI patients (n = 38) both preoperatively and 24 h after PCI, and healthy subjects (n = 20). MPs origins were tested by flow cytometry. Rat thoracic aortas were incubated with MPs to determine the effects of MPs on phosphorylation of endothelial nitric oxide synthase (eNOS), caveolin-1 expression, eNOS association with heat shock protein 90 (Hsp90), generation of nitric oxide (NO) and superoxide anion (O2), and endothelial-dependent vasodilatation.
  
  
  
  Compared with healthy subjects, MP concentrations increased in AMI patients. Undergoing PCI had no further effect on MPs concentration, but it results in increased endothelial-derived MPs proportion and decreased platelet-derived MP ratio. MPs from AMI patients decreased eNOS phosphorylation at Ser1177, increased eNOS phosphorylation at T495 and caveolin-1 expression, decreased eNOS association with Hsp90, decreased NO production but increased (O2) generation, damaged endothelial-dependent vasodilatation. All of these effects of MPs were strengthened by PCI.
  
  
  
  PCI further enhances the vascular injury effect of MPs. Circulating MPs may be a potential therapeutic target for patients undergoing PCI.
authors.affiliation: *Geriatric Vasculocardiology Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China †Department of Children's Cardiac Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumuqi, Xinjiang, China ‡Department of Cardiovascular Medicine, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China §Department of Cardiovascular Medicine, MOE, Ion Channel Disease Laboratory, MOE Key Laboratory of Environment and Genes Related to Diseases, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
authors.forename: Sha
authors.initials: S
authors.lastname: Ye
authors.forename: Xue-Feng
authors.initials: XF
authors.lastname: Shan
authors.forename: Wen-Qi
authors.initials: WQ
authors.lastname: Han
authors.forename: Qian-Rong
authors.initials: QR
authors.lastname: Zhang
authors.forename: Jie
authors.initials: J
authors.lastname: Gao
authors.forename: Ai-Ping
authors.initials: AP
authors.lastname: Jin
authors.forename: Yi
authors.initials: Y
authors.lastname: Wang
authors.forename: Chao-Feng
authors.initials: CF
authors.lastname: Sun
authors.forename: Sui-Long
authors.initials: SL
authors.lastname: Zhang
mesh_terms: D000328:Adult; D000818:Animals; D055252:Cell-Derived Microparticles / Q000378:metabolism / Q000637:transplantation; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000601:surgery; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis*; D062645:Percutaneous Coronary Intervention; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation
chemical_list: D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat