title: Protein analysis of atrial fibrosis via label-free proteomics in chronic atrial fibrillation patients with mitral valve disease.
abstract: BACKGROUND
  Atrial fibrosis, as a hallmark of atrial structure remodeling, plays an important role in maintenance of chronic atrial fibrillation, but interrelationship of atrial fibrosis and atrial fibrillation is uncertain. Label-free proteomics can implement high throughput screening for finding and analyzing pivotal proteins related to the disease.. Therefore, we used label-free proteomics to explore and analyze differentially proteins in chronic atrial fibrillation patients with mitral valve disease.
  
  
  METHODS
  Left and right atrial appendages obtained from patients with mitral valve disease were both in chronic atrial fibrillation (CAF, AF≥6 months, n = 6) and in sinus rhythm (SR, n = 6). One part of the sample was used for histological analysis and fibrosis quantification; other part were analyzed by label-free proteomic combining liquid chromatography with mass spectrometry (LC-MS), we utilized bioinformatics analysis to identify differential proteins.
  
  
  RESULTS
  Degree of atrial fibrosis was higher in CAF patients than that of SR patients. 223 differential proteins were detected between two groups. These proteins mainly had vital functions such as cell proliferation, stress response, focal adhesion apoptosis. We evaluated that serine/threonine protein kinase N2 (PKN2), dermatopontin (DP), S100 calcium binding protein B (S100B), protein tyrosine kinase 2 (PTK2) and discoidin domain receptor tyrosine kinase 2 (DDR2) played important roles in fibrotic process related to atrial fibrillation.
  
  
  CONCLUSIONS
  The study presented differential proteins responsible for atrial fibrosis in chronic atrial fibrillation patients through label-free proteomic analysis. We assessed some vital proteins including their characters and roles. These findings may open up new realm for mechanism research of atrial fibrillation.
authors.affiliation: Cardiovascular Surgery Department, Fuwai Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, People's Republic of China.
authors.forename: Peide
authors.initials: P
authors.lastname: Zhang
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.forename: Xu
authors.initials: X
authors.lastname: Wang
authors.forename: Yunhu
authors.initials: Y
authors.lastname: Song
authors.forename: Yong
authors.initials: Y
authors.lastname: Han
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.forename: Hui
authors.initials: H
authors.lastname: Zhao
mesh_terms: D000328:Adult; D000368:Aged; D020517:Atrial Appendage / Q000378:metabolism / Q000473:pathology; D001281:Atrial Fibrillation / Q000150:complications* / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D005355:Fibrosis; D006349:Heart Valve Diseases / Q000150:complications* / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000473:pathology*; D025941:Protein Interaction Mapping; D060066:Protein Interaction Maps; D020543:Proteome; D040901:Proteomics; D015398:Signal Transduction
chemical_list: D020543:Proteome