title: Agonistic autoantibodies against the angiotensin AT1 receptor increase in unstable angina patients after stent implantation.
abstract: OBJECTIVE
  Agonistic AT1 receptor autoantibodies have been described in patients with hypertension and preeclampsia. These autoantibodies could stimulate proliferation of vascular smooth muscle cells (VSMCs), which are involved in angiotensin II-induced vascular injury in cardiovascular disease. Hence, in this study, we explored the existence of agonistic AT1 receptor autoantibodies in unstable angina (UA) patients and the possible effects of them on the in-stent restenosis of these patients.
  
  
  METHODS
  A total of 95 UA patients and 98 healthy volunteers were enrolled. The serum of each patient was analyzed for the presence of AT1 receptor autoantibodies by enzyme-linked immunosorbent assay. Their effects on VSMC proliferation and c-fos and c-jun expression were studied in vitro.
  
  
  RESULTS
  AT1 receptor autoantibodies were detected in 34/95 patients with UA. The incidence was 10.2% in the control group and rose to 47.37% after stent implantation. In vitro, this autoantibody had agonist-like activity, shown as stimulation of VSMC proliferation and upregulation of c-fos and c-jun expression. These effects were similar to that of angiotensin II and could be weakened partly by the AT1-receptor blocker valsartan.
  
  
  CONCLUSIONS
  Our findings show that the autoantibody from UA patients has similar agonistic activity to angiotensin II and might play a role in the pathogenesis of in-stent restenosis in these patients.
authors.affiliation: aDepartment of Cardiology, Yantai Yu-Huangding Hospital, Medical College of Qing Dao University, Yantai bInstitute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Tian
authors.forename: Li
authors.initials: L
authors.lastname: Sheng
authors.forename: Peng
authors.initials: P
authors.lastname: Huang
authors.forename: Jun
authors.initials: J
authors.lastname: Li
authors.forename: Chuan-Huan
authors.initials: CH
authors.lastname: Zhang
authors.forename: Jun
authors.initials: J
authors.lastname: Yang
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
authors.forename: Liu-Dong
authors.initials: LD
authors.lastname: Li
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000175:diagnosis / Q000276:immunology* / Q000628:therapy*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001323:Autoantibodies / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D049109:Cell Proliferation; D002478:Cells, Cultured; D023903:Coronary Restenosis / Q000175:diagnosis / Q000276:immunology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000295:instrumentation*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000276:immunology*; D015607:Stents; D016896:Treatment Outcome; D015854:Up-Regulation
chemical_list: C544065:AGTR1 protein, human; D047228:Angiotensin II Type 1 Receptor Blockers; D001323:Autoantibodies; D015415:Biomarkers; D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D044140:Receptor, Angiotensin, Type 1