title: Expression of spliceosome assembly factor SC-35 in TUNEL-positive atrial cardiomyocytes in mitral and tricuspid regurgitation: viability of atrial cardiomyocytes.
abstract: BACKGROUND
  Most of the atrial cardiomyocytes with positive terminal deoxynucleotidyl transferase (TdT)-mediated dUTP in situ nick end-labelling (TUNEL) reaction are not apoptotic in patients with mitral and tricuspid valve diseases. The TUNEL-positive myocytes with expression of spliceosome assembly factor SC-35, an indicator of increased RNA synthesis, should be living cardiomyocytes.
  
  
  METHODS
  This study analyzed twenty-three patients with significant mitral and tricuspid regurgitation. Fifteen patients had persistent atrial fibrillation, and eight had sinus rhythm. Atrial appendageal tissues were obtained during surgery. Immunohistochemical study was performed.
  
  
  RESULTS
  Immunohistochemical study of fibrillating right atrial myocardium demonstrated that 44.8 ± 24.6% of myocytes had TUNEL-positive nuclei whereas 39.4 ± 21.4% of myocytes had TUNEL-positive nuclei in sinus right atrial myocardium (p=0.682). However, most (81.6%) nuclei of TUNEL-positive myocytes in the fibrillating right atria also expressed proliferating cell nuclear antigen (PCNA), an indicator of DNA replication and repair, and most nuclei (91.8%) of TUNEL-positive myocytes also expressed SC-35. In fibrillating left atria, most (88.1%) nuclei of TUNEL-positive myocytes also expressed SC-35. Similarly, in sinus right atrial myocardium, most (78.0%) nuclei of TUNEL-positive myocytes expressed PCNA, and most (91.4%) nuclei of TUNEL-positive myocytes also expressed SC-35, but none expressed Ki-67, a replication-associated antigen. Additionally, the percentage of TUNEL-positive myocytes in the right atria significantly and positively correlated with the percentage of PCNA-positive myocytes (r=0.826, p<0.001) and SC-35 positive myocytes (r=0.713, p<0.001).
  
  
  CONCLUSIONS
  Most TUNEL-positive atrial cardiomyocytes in patients with mitral and tricuspid regurgitation are living cardiomyocytes.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Taiwan, ROC. chenmien@ms76.hinet.net
authors.forename: Mien-Cheng
authors.initials: MC
authors.lastname: Chen
authors.forename: Jen-Ping
authors.initials: JP
authors.lastname: Chang
authors.forename: Wan-Chun
authors.initials: WC
authors.lastname: Ho
authors.forename: Wen-Hao
authors.initials: WH
authors.lastname: Liu
authors.forename: Chien-Jen
authors.initials: CJ
authors.lastname: Chen
authors.forename: Cheng-Hsu
authors.initials: CH
authors.lastname: Yang
authors.forename: Yung-Lung
authors.initials: YL
authors.lastname: Chen
authors.forename: Tzu-Hsien
authors.initials: TH
authors.lastname: Tsai
mesh_terms: D000328:Adult; D000368:Aged; D020517:Atrial Appendage / Q000378:metabolism / Q000473:pathology; D002470:Cell Survival / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D020287:In Situ Nick-End Labeling / Q000379:methods*; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D009687:Nuclear Proteins / Q000096:biosynthesis* / Q000172:deficiency / Q000235:genetics; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis; D012261:Ribonucleoproteins / Q000096:biosynthesis* / Q000235:genetics; D000068103:Serine-Arginine Splicing Factors; D017381:Spliceosomes / Q000378:metabolism*; D014262:Tricuspid Valve Insufficiency / Q000235:genetics / Q000378:metabolism* / Q000473:pathology
chemical_list: D019394:Ki-67 Antigen; D009687:Nuclear Proteins; D018809:Proliferating Cell Nuclear Antigen; D012261:Ribonucleoproteins; C073288:SRSF2 protein, human; D000068103:Serine-Arginine Splicing Factors