Brief Reviews |
From the A.I. Virtanen Institute (M.O.H., S.Y.-H.) and Department of Medicine (S.Y.-H.), University of Kuopio, and Gene Therapy Unit (S.Y.-H.), Kuopio University Hospital, Kuopio, Finland.
Correspondence to Seppo Ylä-Herttuala, MD, PhD, Department of Molecular Medicine, A.I. Virtanen Institute, University of Kuopio, PO Box 1627, FIN-70211, Kuopio, Finland. E-mail Seppo.Ylaherttuala{at}uku.fi
Series Editor: Giulio Gabbiani
ATVB in Focus
Smooth Muscle Cells
Previous Brief Reviews in this Series:
Hillebrands J-L, Klatter FA, Rozing J. Origin of vascular smooth muscle cells and the role of circulating stem cells in transplant arteriosclerosis. 2003;23:380387.
Iso T, Hamamori Y, Kedes L. Notch signaling in vascular development. 2003;23:543553.
Kumar MS, Owens GK. Combinatorial control of smooth muscle-specific gene expression. 2003;23:737747.
Hao H, Gabbiani G, Bochaton-Piallat M-L. Arterial smooth muscle cell heterogeneity: Implications for atherosclerosis and restenosis development 2003;23:15101520.
DNA methylation is a form of epigenetic modification of the genome that can regulate gene expression. Hypermethylation of CpG islands in the promoter areas leads to decreased gene expression, whereas promoters of actively transcribed genes remain nonmethylated. Because of cellular proliferation and monoclonality of at least some of the lesion cells, atherosclerotic lesions have been compared with benign vascular tumors.1,2 However, although genetic and epigenetic background favors neoplastic transformation, atherosclerotic plaques never develop to malignant tumors. Among cancer cells, common features are genome-wide hypomethylation, which correlates with transformation and tumor progression. Recent studies have shown that DNA methylation changes occur also during atherogenesis and may contribute to the lesion development.
Key Words: atherogenesis DNA methylation 5-methylcytosine epigenetic gene regulation gene expression
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