title: Gene expression signatures differ with extent of atherosclerosis in monkey iliac artery.
abstract: OBJECTIVE
  The aim of this study was to evaluate global gene expression patterns in the common iliac arteries of monkeys with a varied extent of atherosclerosis.
  
  
  METHODS
  The left common iliac artery was removed from ovariectomized cynomolgus monkeys (n = 12) after 6.5 years of consuming a diet containing fat and cholesterol at levels comparable with those consumed in Western populations. Arterial gene expression was analyzed using DNA microarray and real-time reverse transcription-polymerase chain reaction.
  
  
  RESULTS
  Significant differential expression of 986 genes was observed in iliac arteries containing moderate to large atherosclerotic plaques compared with normal/minimally affected reference group arteries. Atherosclerosis-associated genes included cytokines, chemokines, components of signal transduction pathways, and transcriptional activators and repressors, as well as other functional categories. Real-time reverse transcription-polymerase chain reaction confirmed a differential expression of genes chosen from a variety of functional categories. Specifically, the expression of genes for estrogen receptor-1, claudin 11, and brain heart protocadherin 7 was reduced, whereas the expression of genes for apolipoprotein E, growth differentiation factor 15, superoxide dismutase-2, SET domain bifurcated 2, phospholipase A2 group IIA, phospholipase A2 group VII, and ring finger protein 149 was increased in atherosclerotic arteries.
  
  
  CONCLUSIONS
  The gene expression environment in arteries containing atherosclerotic plaques is profoundly different from that of relatively unaffected arteries and reflects the cellular and molecular complexity of atherosclerosis and associated arterial remodeling processes.
authors.affiliation: Division of Basic Biomedical Sciences, Sanford School of Medicine, Universityof South Dakota, Vermillion, SD 57069, USA. Kathleen.Eyster@usd.edu
authors.forename: Kathleen M
authors.initials: KM
authors.lastname: Eyster
authors.forename: Susan E
authors.initials: SE
authors.lastname: Appt
authors.forename: Connie J
authors.initials: CJ
authors.lastname: Mark-Kappeler
authors.forename: Abha
authors.initials: A
authors.lastname: Chalpe
authors.forename: Thomas C
authors.initials: TC
authors.lastname: Register
authors.forename: Thomas B
authors.initials: TB
authors.lastname: Clarkson
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000096:biosynthesis / Q000235:genetics; D050197:Atherosclerosis / Q000235:genetics* / Q000503:physiopathology; D015820:Cadherins / Q000096:biosynthesis / Q000235:genetics; D057167:Claudins / Q000096:biosynthesis / Q000235:genetics; D004041:Dietary Fats / Q000009:adverse effects; D004195:Disease Models, Animal; D047628:Estrogen Receptor alpha / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D020869:Gene Expression Profiling; D055436:Growth Differentiation Factor 15 / Q000096:biosynthesis / Q000235:genetics; D011495:Histone-Lysine N-Methyltransferase / Q000096:biosynthesis / Q000235:genetics; D007083:Iliac Artery / Q000378:metabolism* / Q000503:physiopathology; D008252:Macaca fascicularis; D010052:Ovariectomy; D054467:Phospholipases A2 / Q000096:biosynthesis / Q000235:genetics; D013482:Superoxide Dismutase / Q000096:biosynthesis / Q000235:genetics; D000099156:Superoxide Dismutase 2
chemical_list: D001057:Apolipoproteins E; D015820:Cadherins; D057167:Claudins; D004041:Dietary Fats; D047628:Estrogen Receptor alpha; D055436:Growth Differentiation Factor 15; D011495:Histone-Lysine N-Methyltransferase; D054467:Phospholipases A2; D013482:Superoxide Dismutase; D000099156:Superoxide Dismutase 2