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(Circulation. 2003;108:1845.)
© 2003 American Heart Association, Inc.

Clinical Investigation and Reports

Physiological Genomics of Human Arteries

Quantitative Relationship Between Gene Expression and Arterial Stiffness

Séverine Durier, PhD^*; Céline Fassot, PhD^*; Stéphane Laurent, MD, PhD; Pierre Boutouyrie, MD, PhD; Jean-Paul Couetil, MD; Erika Fine, MD; Patrick Lacolley, MD, PhD; Victor J. Dzau, MD; Richard E. Pratt, PhD

From the Laboratory of Physiological Genomics, Department of Medicine (V.J.D., R.E.P.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; the Department of Pharmacology and INSERM EMI 107 (S.D., C.F., S.L., P.B., E.F., P.L.) and the Department of Cardiac Surgery (J.-P.C.), Hôpital Européen Georges Pompidou, Paris, France

Correspondence to Richard E. Pratt, PhD, Department of Medicine, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail rpratt{at}rics.bwh.harvard.edu

Received November 18, 2002; de novo received May 22, 2003; revision received July 24, 2003; accepted July 26, 2003.

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.

Methods and 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.

Conclusion— 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.

Key Words: arteries • extracellular matrix • phosphoprotein phosphatase • proteins, cytoskeletal • genomics

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