title: Proteomic study reveals plasma protein changes in congenital heart diseases.
abstract: BACKGROUND
  Congenital heart disease (CHD) is the most common birth defect in newborns. Plasma proteins may serve as indicators of disease and are a rich source for biomarker discovery, but little has been studied in CHD. We examined the hypothesis that plasma proteins may be altered and related to the pathologic changes of CHD.
  
  
  METHODS
  Differential protein analysis was performed in the plasma of patients with tetralogy of Fallot, isolated ventricular septal defect, and normal controls by using two-dimensional electrophoresis and mass spectrometry. Candidate proteins that might be related to disease processes were further confirmed by enzyme-linked immunosorbent assay in the new samples (n=40).
  
  
  RESULTS
  Identified were 18 differentially expressed protein spots and 10 corresponding proteins or polypeptides. Among those, 2 downregulated proteins, gelsolin, ficolin-3, with significant clinical relevance, were further analyzed for validation. The plasma levels of gelsolin (76.30±4.42 vs 131.80±23.46 μg/mL in control; p=0.025, n=40 in each group) and ficolin-3 (4.93±0.36 vs 10.58±1.58 μg/mL in control; p=0.001, n=40 in each group) in tetralogy patients were significantly lower than those in normal controls. The ficolin-3 plasma level was also lower in the patients with isolated VSD (5.55±0.34 vs 10.58±1.58 μg/mL in control μg/mL; p=0.003, n=40 in each group).
  
  
  CONCLUSIONS
  We used proteomic methods to demonstrate for the first time the plasma protein changes in CHD patients that may reveal the possible mechanisms for the prolonged bleeding time in tetralogy patients and the susceptibility to pulmonary infections in patients with CHDs. These findings have strong clinical implications.
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin and The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Xuan
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin, China.
authors.forename: Ge
authors.initials: G
authors.lastname: Gao
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin and The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China; Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Yang
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin, China.
authors.forename: Xiu-Li
authors.initials: XL
authors.lastname: Wang
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin, China.
authors.forename: Zhi-Gang
authors.initials: ZG
authors.lastname: Liu
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin, China.
authors.forename: Xiao-Cheng
authors.initials: XC
authors.lastname: Liu
authors.affiliation: TEDA International Cardiovascular Hospital, Tianjin and The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China; Department of Surgery, Oregon Health and Science University, Portland, Oregon. Electronic address: gwhezj@163.com.
authors.forename: Guo-Wei
authors.initials: GW
authors.lastname: He
mesh_terms: D001798:Blood Proteins / Q000235:genetics*; D002675:Child, Preschool; D005260:Female; D006330:Heart Defects, Congenital / Q000097:blood* / Q000235:genetics*; D006801:Humans; D008297:Male; D040901:Proteomics
chemical_list: D001798:Blood Proteins