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Our understanding of the pathophysiology of hypertension is limited by a lack of information regarding gene expression in vascular smooth muscle (VSMC). To address this issue, we used cDNA microarrays to assess gene expression changes in VSMC in response to a physiological agonist of VSMC, serotonin, and a cyclooxygenase (COX) product, prostaglandin (PG)H2. COX inhibitors were used to verify the identity of the genes regulated by serotonin and PGH2. Fluorescent intensities of mRNAs were measured using the GenePix 4000B scanner. Gene expression was compared among the following groups of samples: untreated, serotonin-stimulated, serotonin-and-COX-1 inhibitor, serotonin-and-COX-2 inhibitor, PGH2-stimulated, and PGH2-and-COX-1 inhibitor. Many of the gene products represented on the microarrays have been shown to have functions relevant to VSMC biology. Genes regulated by serotonin or PGH2 included those encoding cell-cell and cell-matrix adhesion molecules and several transcription factors. Genes regulated by either serotonin or PGH2 and inhibited by the COX inhibitors included the transcription factors PDGF-A, AP-1, and E2F-3; the cytokines IL-6, IL-1alpha, and MCP-1; the platelet-derived growth factor receptor beta; and the genes encoding the VSMC-specific contractile proteins, calponin, calretinin, and alpha-actinin, among others. These data suggest that vasoconstrictor (serotonin) and vasodilator (PGH2) signaling pathways in VSMC differentially regulate expression of genes that mediate the regulation of cell proliferation and motility. These data also demonstrate a novel method of analysis of gene expression of genes in VSMC.Q:
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