title: Telomere shortening in human coronary artery diseases.
abstract: BACKGROUND
  Increased cell turnover in response to injury is considered to be important in the development of atherosclerotic plaques. Telomere shortening has been shown to be associated with cell turnover. We assessed the telomere length of human coronary endothelial cells to clarify whether there is a relationship between telomere shortening and coronary artery disease (CAD).
  
  
  RESULTS
  Coronary endothelial cells were obtained from 11 patients with CAD who underwent autopsy and 22 patients without CAD who underwent autopsy by scraping off the luminal surface of coronary arteries. DNA extracted from the endothelial cells were blotted and hybridized with telomere-specific oligonucleotide ([TTAGGG]4). The hybridization signal intensity, which represented telomeric DNA content, was standardized with centromeric DNA content (T/C ratio) to estimate telomere length. The T/C ratios were significantly smaller (P<0.0001) in CAD patients than in age-matched non-CAD patients (CAD patients, 0.462+/-0.135; non-CAD patients, 1.002+/-0.212). In 6 individual CAD patients, the T/C ratio at the atherosclerotic lesion was significantly smaller (P<0.05) than that at the non-atherosclerotic portion.
  
  
  CONCLUSIONS
  These findings suggest that focal replicative senescence and telomere shortening of endothelial cells may play a critical role in coronary atherogenesis and CAD.
authors.affiliation: Department of Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
authors.forename: Masayuki
authors.initials: M
authors.lastname: Ogami
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ikura
authors.forename: Masahiko
authors.initials: M
authors.lastname: Ohsawa
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Matsuo
authors.forename: Soichiro
authors.initials: S
authors.lastname: Kayo
authors.forename: Noriko
authors.initials: N
authors.lastname: Yoshimi
authors.forename: Eishu
authors.initials: E
authors.lastname: Hai
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Shirai
authors.forename: Shoichi
authors.initials: S
authors.lastname: Ehara
authors.forename: Ryushi
authors.initials: R
authors.lastname: Komatsu
authors.forename: Takahiko
authors.initials: T
authors.lastname: Naruko
authors.forename: Makiko
authors.initials: M
authors.lastname: Ueda
mesh_terms: D000368:Aged; D002455:Cell Division; D002478:Cells, Cultured / Q000737:chemistry; D016922:Cellular Senescence; D003324:Coronary Artery Disease / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D004247:DNA / Q000032:analysis; D042783:Endothelial Cells / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D005347:Fibroblasts / Q000737:chemistry; D006801:Humans; D008297:Male; D008875:Middle Aged; D016615:Telomere / Q000648:ultrastructure*
chemical_list: D004247:DNA