title: Physiological genomics of human arteries: quantitative relationship between gene expression and arterial stiffness.
abstract: BACKGROUND
  Previous genomic studies with human tissues have compared differential gene expression between 2 conditions (ie, normal versus diseased) to identify altered gene expression in a binary manner; however, a potentially more informative approach is to correlate the levels of gene expression with quantitative physiological parameters.
  
  
  RESULTS
  In this study, we have used this approach to examine genes whose expression correlates with arterial stiffness in human aortic specimens. Our data identify 2 distinct groups of genes, those associated with cell signaling and those associated with the mechanical regulation of vascular structure (cytoskeletal-cell membrane-extracellular matrix). Although previous studies have concentrated on the contribution of the latter group toward arterial stiffness, our data suggest that changes in expression of signaling molecules play an equally important role. Alterations in the profiles of signaling molecules could be involved in the regulation of cell cytoskeletal organization, cell-matrix interactions, or the contractile state of the cell.
  
  
  CONCLUSIONS
  Although the influence of smooth muscle contraction/relaxation on arterial stiffness could be controversial, our provocative data would suggest that further studies on this subject are indicated.
authors.affiliation: Department of Pharmacology and INSERM EMI 107, Paris, France.
authors.forename: Séverine
authors.initials: S
authors.lastname: Durier
authors.forename: Céline
authors.initials: C
authors.lastname: Fassot
authors.forename: Stéphane
authors.initials: S
authors.lastname: Laurent
authors.forename: Pierre
authors.initials: P
authors.lastname: Boutouyrie
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Couetil
authors.forename: Erika
authors.initials: E
authors.lastname: Fine
authors.forename: Patrick
authors.initials: P
authors.lastname: Lacolley
authors.forename: Victor J
authors.initials: VJ
authors.lastname: Dzau
authors.forename: Richard E
authors.initials: RE
authors.lastname: Pratt
mesh_terms: D000368:Aged; D001011:Aorta / Q000378:metabolism* / Q000648:ultrastructure; D001161:Arteriosclerosis / Q000235:genetics* / Q000473:pathology; D001794:Blood Pressure; D003324:Coronary Artery Disease / Q000235:genetics / Q000473:pathology; D003598:Cytoskeletal Proteins / Q000096:biosynthesis / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D023281:Genomics; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis / Q000235:genetics; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D011509:Proteoglycans / Q000096:biosynthesis / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics; D014158:Transcription, Genetic; D014655:Vascular Resistance / Q000235:genetics; D014661:Vasoconstriction / Q000235:genetics
chemical_list: D003598:Cytoskeletal Proteins; D016326:Extracellular Matrix Proteins; D008565:Membrane Proteins; D011509:Proteoglycans