title: Increased p53 protein expression in human failing myocardium.
abstract: BACKGROUND
  The p53 gene is a tumor-suppressor gene which involves apoptosis and cell-cycle arrest under certain stress stimulate. However, the status of the p53 gene expression in human myocardium in congestive heart failure (CHF) remains unclear. Therefore, the current study was designed to investigate the expression of the p53 protein in human myocardium in normal subjects and in patients with severe CHF.
  
  
  METHODS
  Human ventricular cardiac tissue was obtained from 7 normal subjects and 7 end-stage CHF patients during cardiac transplantation. The expression of p53 protein was determined by immunohistochemical staining. The cardiac apoptosis was determined by TUNEL staining.
  
  
  RESULTS
  The p53 protein was minimally stained in normal human ventricular cardiomyocytes. In contrast, the staining density and positive stained nuclear (%) of p53 was significantly increased in ventricular cardiomyocytes of patients with severe CHF. Apoptosis in CHF human myocardium also markedly increased.
  
  
  CONCLUSIONS
  The significantly increased expression of p53 in CHF human cardiomyocytes suggests that p53 may play an important pathophysiological role in the process of CHF through mechanisms involving myocardial apoptosis.
authors.affiliation: Department of Surgery, University of Maryland School of Medicine, Baltimore, USA.
authors.forename: H
authors.initials: H
authors.lastname: Song
authors.forename: J V
authors.initials: JV
authors.lastname: Conte
authors.forename: A H
authors.initials: AH
authors.lastname: Foster
authors.forename: J S
authors.initials: JS
authors.lastname: McLaughlin
authors.forename: C
authors.initials: C
authors.lastname: Wei
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000235:genetics; D015415:Biomarkers; D002455:Cell Division / Q000235:genetics; D004247:DNA / Q000235:genetics; D053938:DNA Fragmentation; D006333:Heart Failure / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D016027:Heart Transplantation; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006801:Humans; D020287:In Situ Nick-End Labeling; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D015415:Biomarkers; D016159:Tumor Suppressor Protein p53; D004247:DNA