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    Multi-organ expression profiling uncovers a gene module in coronary artery disease involving transendothelial migration of leukocytes and LIM domain binding 2: The Stockholm Atherosclerosis Gene Expression (STAGE) study

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    Type
    Article
    Authors
    Hägg, Sara
    Skogsberg, Josefin
    Lundström, Jesper
    Noori, Peri
    Nilsson, Roland
    Zhong, Hua
    Maleki, Shohreh
    Shang, Ming-Mei
    Brinne, Björn
    Bradshaw, Maria
    Bajic, Vladimir B. cc
    Samnegård, Ann
    Silveira, Angela
    Kaplan, Lee M.
    Gigante, Bruna
    Leander, Karin
    de Faire, Ulf
    Rosfors, Stefan
    Lockowandt, Ulf
    Liska, Jan
    Konrad, Peter
    Takolander, Rabbe
    Franco-Cereceda, Anders
    Schadt, Eric E.
    Ivert, Torbjörn
    Hamsten, Anders
    Tegnér, Jesper
    Björkegren, Johan
    KAUST Department
    Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
    Computational Bioscience Research Center (CBRC)
    Applied Mathematics and Computational Science Program
    Date
    2009-12-04
    Permanent link to this record
    http://hdl.handle.net/10754/325276
    
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    Abstract
    Environmental exposures filtered through the genetic make-up of each individual alter the transcriptional repertoire in organs central to metabolic homeostasis, thereby affecting arterial lipid accumulation, inflammation, and the development of coronary artery disease (CAD). The primary aim of the Stockholm Atherosclerosis Gene Expression (STAGE) study was to determine whether there are functionally associated genes (rather than individual genes) important for CAD development. To this end, two-way clustering was used on 278 transcriptional profiles of liver, skeletal muscle, and visceral fat (n =66/tissue) and atherosclerotic and unaffected arterial wall (n =40/tissue) isolated from CAD patients during coronary artery bypass surgery. The first step, across all mRNA signals (n =15,042/12,621 RefSeqs/genes) in each tissue, resulted in a total of 60 tissue clusters (n= 3958 genes). In the second step (performed within tissue clusters), one atherosclerotic lesion (n =49/48) and one visceral fat (n =59) cluster segregated the patients into two groups that differed in the extent of coronary stenosis (P=0.008 and P=0.00015). The associations of these clusters with coronary atherosclerosis were validated by analyzing carotid atherosclerosis expression profiles. Remarkably, in one cluster (n =55/54) relating to carotid stenosis (P =0.04), 27 genes in the two clusters relating to coronary stenosis were confirmed (n= 16/17, P<10 -27and-30). Genes in the transendothelial migration of leukocytes (TEML) pathway were overrepresented in all three clusters, referred to as the atherosclerosis module (A-module). In a second validation step, using three independent cohorts, the Amodule was found to be genetically enriched with CAD risk by 1.8-fold (P<0.004). The transcription co-factor LIM domain binding 2 (LDB2) was identified as a potential high-hierarchy regulator of the A-module, a notion supported by subnetwork analysis, by cellular and lesion expression of LDB2, and by the expression of 13 TEML genes in Ldb2-deficient arterial wall. Thus, the A-module appears to be important for atherosclerosis development and, together with LDB2, merits further attention in CAD research. 2009 Hgg et al.
    Citation
    Hägg S, Skogsberg J, Lundström J, Noori P, Nilsson R, et al. (2009) Multi-Organ Expression Profiling Uncovers a Gene Module in Coronary Artery Disease Involving Transendothelial Migration of Leukocytes and LIM Domain Binding 2: The Stockholm Atherosclerosis Gene Expression (STAGE) Study. PLoS Genet 5: e1000754. doi:10.1371/journal.pgen.1000754.
    Publisher
    Public Library of Science (PLoS)
    Journal
    PLoS Genetics
    DOI
    10.1371/journal.pgen.1000754
    PubMed ID
    19997623
    PubMed Central ID
    PMC2780352
    ae974a485f413a2113503eed53cd6c53
    10.1371/journal.pgen.1000754
    Scopus Count
    Collections
    Articles; Applied Mathematics and Computational Science Program; Computational Bioscience Research Center (CBRC); Computer, Electrical and Mathematical Science and Engineering (CEMSE) Division

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