on February 2, 2006
Published online before print February 2, 2006, doi: 10.1161/01.ATV.0000208185.16371.97
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Submitted on November 15, 2005
Accepted on January 18, 2006
Molecular Signatures Determining Coronary Artery and Saphenous Vein Smooth Muscle Cell Phenotypes. Distinct Responses to Stimuli
David Xing-Fei Deng *;
From Agilent Laboratories (D.X.-F.D., A.T., A.V., A.B.-D., Z.Y., L.B.), Palo Alto, Calif; and Donald W. Reynolds Cardiovascular Clinical Research Center (J.M.S., P.T., T.Q.), Stanford University School of Medicine, California.
* To whom correspondence should be addressed. E-mail: david_deng{at}agilent.com.
Objectives--We compared gene expression profiles and functional responses to oxidized low-density lipoprotein (LDL) and platelet-derived growth factor (PDGF) between cultured smooth muscle cells (SMCs) from human coronary artery (CASMs) and saphenous vein (SVSMs) to better understand the molecular mechanisms underlying functional differences among distinct SMC subtypes.
Methods and Results--Oxidized LDL (OxLDL) and PDGF elicited markedly different functional responses and expression profiles between the 2 SMC subtypes. In CASMs, OxLDL inhibited cell proliferation and migration and modified gene expression of some chemokines, proinflammatory cytokines, insulin-like growth factor binding proteins (IGFBPs), and endothelial and smooth muscle marker genes. In SVSMs, OxLDL promoted proliferation partially via, insulin-like growth factor-1 signaling, activated nuclear factor 
B and phosphatidylinositol signaling pathways, and upregulated prostaglandin receptors and synthases. In untreated cells, 
-chemokines, proinflammatory cytokines, and genes associated with lipid biosynthesis were higher in CASMs, whereas some 
-chemokines, metalloproteinase inhibitors, and IGFBPs were higher in SVSMs. Interestingly, the basal expression levels of these genes seemed closely related to their responses to OxLDL and PDGF.
Conclusions--Our results reveal molecular signatures that define the distinct phenotypes characteristics of coronary artery and SVSM subtypes.
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