Research conducted at University of Heidelberg has provided new information about atherosclerosis
2008 JAN 14 -- "During the early phase of atherosclerosis, T cells and monocytes attach to and migrate through the endothelium into the vessel wall. To provide an insight into the potential cross talk between T cells and smooth muscle cells (SMC) in atherogenesis, we investigated changes in gene expression caused by CD40 ligation in cultured vascular SMC and their consequences for monocyte activation," scientists in Heidelberg, Germany report. "CD40 expression in human-cultured SMC was induced by 24h treatment with tumor necrosis factor-alpha plus interferon-gamma followed by 12-h exposure to mouse myeloma cells stably expressing human CD 154 or the cot-responding control cells. DNA microarray analysis (Affymetrix HG-U952A chip) indicated 33 up-regulated genes in three individual experiments of which 19 encoded pro-inflammatory adhesion molecules, cytokines, chemokines, and receptors. One functional consequence of this change in gene expression was an activation of transformed human prornonocytic- I monocytes exposed to the conditioned medium of the stimulated SMC. Subsequent antibody neutralization experiments identified granulocyte-macropbage colony-stimulating factor (GM-CSF) as the SNIC-derived cytokine responsible for this effect. Thus, vascular SNIC-like endothelial cells appear to contribute to the maintenance of an inflammatory response in the atherosclerotic vessel wall upon CD40-CD154 co-stimulation," wrote M. Stojakovic and colleagues, University of Heidelberg. The researchers concluded: "Among 19 up-regulated pro-inflammatory gene products, GM-CSF plays an important role in SMC-dependent monocyte activation." Stojakovic and colleagues published their study in the Journal of Molecular Medicine - Jmm (CD154-stimulated GM-CSF release by vascular smooth muscle cells elicits monocyte activation - role in atherogenesis. Journal of Molecular Medicine - Jmm, 2007;85(11):1229-1238). For additional information, contact M. Hecker, University of Heidelberg, Division Cardiovascular Physiol, Institute Physiol & Pathophysiology, Neuenheimer Feld 326, D-69120 Heidelberg, Germany. The publisher's contact information for the Journal of Molecular Medicine - Jmm is: Springer, 233 Spring Street, New York, NY 10013, USA. Keywords: Germany, Heidelberg, Angiology, Atherosclerosis, Biotechnology, DNA, DNA Microarray, DNA Research, Endothelium, Immunology, Interferon, Interferon Gamma, Medical Device, Molecular Medicine, Myeloma, Necrosis, University of Heidelberg. This article was prepared by Proteomics Weekly editors from staff and other reports. Copyright 2008, Proteomics Weekly via NewsRx.com.
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