title: Correlations between clinical variables and gene-expression profiles in carotid plaque instability.
abstract: OBJECTIVE
  Strokes, a major cause of disability, are often caused by embolism from unstable carotid plaques. The aim of this study was to validate a biobank of human carotid endarterectomies as a platform for further exploration of pathways for plaque instability. For this purpose, we investigated the relationship between clinical parameters of plaque instability and expression of genes previously shown to be associated with either plaque instability or healing processes in the vessel wall.
  
  
  METHODS
  A database of clinical information and gene-expression microarray data from 106 carotid endarterectomies were used.
  
  
  RESULTS
  Expression of matrix metalloproteinase (MMP)-9 and MMP-7 was 100-fold higher in plaques than in normal artery. In general, genes associated with inflammation (such as RANKL and CD68) were overexpressed in symptomatic compared with asymptomatic plaques. Plaques obtained from patients undergoing surgery within 2 weeks after an embolic event showed up-regulation of genes involved in healing reactions in the vessel wall (including elastin and collagen). Statin treatment, as well as echodense lesions, were associated with a more stable phenotype.
  
  
  CONCLUSIONS
  Here, we demonstrate that gene-expression profiles reflect clinical parameters. Our results suggest that microarray technology and clinical variables can be used for the future identification of central molecular pathways in plaque instability.
authors: Center for Molecular Medicine and Division of Vascular Surgery, Department of Molecular Medicine and Surgery, Karolinska University Hospital Solna and Karolinska Institutet, Stockholm, Sweden. Anton.Razuvaev@ki.se
authors: A
authors: A
authors: Razuvaev
authors: J
authors: J
authors: Ekstrand
authors: L
authors: L
authors: Folkersen
authors: H
authors: H
authors: Agardh
authors: D
authors: D
authors: Markus
authors: J
authors: J
authors: Swedenborg
authors: G K
authors: GK
authors: Hansson
authors: A
authors: A
authors: Gabrielsen
authors: G
authors: G
authors: Paulsson-Berne
authors: J
authors: J
authors: Roy
authors: U
authors: U
authors: Hedin
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000235:genetics; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics; D016893:Carotid Stenosis / Q000235:genetics* / Q000601:surgery; D003094:Collagen / Q000235:genetics; D030541:Databases, Genetic; D004549:Elastin / Q000235:genetics; D016894:Endarterectomy, Carotid; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D020766:Intracranial Embolism / Q000235:genetics*; D008297:Male; D020783:Matrix Metalloproteinase 7 / Q000235:genetics; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D010641:Phenotype; D053245:RANK Ligand / Q000235:genetics; D013223:Statistics as Topic; D013548:Sweden; D015854:Up-Regulation / Q000235:genetics; D014945:Wound Healing / Q000235:genetics; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D003094:Collagen; D004549:Elastin; D020783:Matrix Metalloproteinase 7; D020780:Matrix Metalloproteinase 9; D053245:RANK Ligand; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C505688:TNFSF11 protein, human; C060932:MMP7 protein, human