title: Evidence of apoptosis in human carotid atheroma.
abstract: OBJECTIVE
  Apoptosis is a morphologically distinct form of programmed cell death that plays a major role in cellular development and homeostasis. In this study, we examined the role that apoptosis may have in the pathogenesis of atherosclerosis.
  
  
  METHODS
  We examined immunohistochemically 20 normal carotid arteries and the carotid arteries of 86 patients (mean age, 68 years; range, 52 to 80 years) who underwent atherectomy for primary atherosclerosis. The expression of two genes, BCL2, which inhibits apoptosis, and BAX, which induces apoptosis, was examined and correlated to the presence of risk factors that included hypertension, smoking, hyperlipidemia, and diabetes mellitus.
  
  
  RESULTS
  BAX expression was found in 26 of 86 cases (30%), and no immunoreactivity was found in the normal carotid specimens. BCL2 expression was not seen in any examined tissues (atherosclerotic or normal carotid arteries). Of the 26 patients who expressed the BAX gene, 22 were hypertensive (85%), and hypertension (>160/95 mm Hg) was present in 25 of 60 patients (41%) who did not express the BAX gene (p < 0.01). No significant correlation was found between the expression of the BAX gene and other risk factors (smoking, hyperlipidemia, diabetes mellitus) or presenting symptoms.
  
  
  CONCLUSIONS
  In a significant number of stenosed carotid arteries (30%), we found no evidence of apoptosis suggested by the presence of BAX expression. Hypertension was more prevalent in those patients with BAX gene expression than in those patients without BAX gene expression. BCL2 expression, which inhibits apoptosis, was not found. Further study of this phenomenon may contribute to the discovery of new treatments for atherosclerosis.
authors.affiliation: Molecular Immunology Laboratory, Medical School of Athens, Hippokration Hospital, Greece.
authors.forename: M M
authors.initials: MM
authors.lastname: Konstadoulakis
authors.forename: G D
authors.initials: GD
authors.lastname: Kymionis
authors.forename: M
authors.initials: M
authors.lastname: Karagiani
authors.forename: V
authors.initials: V
authors.lastname: Katergianakis
authors.forename: N
authors.initials: N
authors.lastname: Doundoulakis
authors.forename: V
authors.initials: V
authors.lastname: Pararas
authors.forename: A
authors.initials: A
authors.lastname: Koutselinis
authors.forename: M
authors.initials: M
authors.lastname: Sehas
authors.forename: P
authors.initials: P
authors.lastname: Peveretos
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000235:genetics; D001161:Arteriosclerosis / Q000209:etiology / Q000235:genetics / Q000473:pathology*; D002339:Carotid Arteries / Q000166:cytology; D016893:Carotid Stenosis / Q000209:etiology / Q000235:genetics / Q000473:pathology*; D016923:Cell Death / Q000235:genetics; D002468:Cell Physiological Phenomena; D016009:Chi-Square Distribution; D004396:Coloring Agents; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000235:genetics; D016894:Endarterectomy, Carotid; D005786:Gene Expression Regulation; D019254:Genes, bcl-2 / Q000235:genetics; D006706:Homeostasis / Q000235:genetics / Q000502:physiology; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000235:genetics; D006973:Hypertension / Q000150:complications / Q000235:genetics; D007150:Immunohistochemistry; D008875:Middle Aged; D015995:Prevalence; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects / Q000235:genetics; D051028:bcl-2-Associated X Protein
chemical_list: C494826:BAX protein, human; D004396:Coloring Agents; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein