Chemokines, or chemotactic cytokines, are a family of cytokines that act as attractant molecules for leukocytes and which have an emerging role in atherosclerosis (Reape and Groot 1999). The chemokine receptor CCR5 has been identified in vascular smooth muscle cells (Schecter et al., 2000), perhaps suggesting ligands of this receptor, such as MIP-1β (macrophage inflammatory protein-1 β, or CCL4), may also have a vascular localisation. MIP-1β is chemoattractant for monocytes and T-cells and has a potential role in atherosclerotic lesion development. This is supported by localisation studies in animal models (Lutgens et al., 2005) however localisation in human vasculature has yet to be characterised. The aim of this study was therefore to investigate the distribution of MIP-1β in a panel of human vessels. Messenger RNA (mRNA) was extracted from the smooth muscle layer of human vessels including saphenous vein and aorta and reverse transcribed. PCR was performed with MIP-1β specific primers as used by Krzysiek et al., 1999. For immunocytochemistry, 30 µm sections of human vessels including saphenous vein, normal and diseased coronary artery, left internal mammary artery, radial artery and aorta, were incubated with rabbit anti-MIP-1β antisera (Abcam plc, UK) and detection was via an avidin-biotin method. PCR products corresponding to the expected size for MIP-1β cDNA were detected in arterial and venous smooth muscle, indicating the cellular expression of the MIP-1β transcript. Expression at the protein level was shown by immunocytochemical staining in all tissues tested. These data demonstrate the expression of MIP-1β at both the mRNA and the protein level in all vessels investigated, suggesting widespread vascular distribution. This builds upon previous work in animal tissues to indicate a potential role for MIP-1β in human atherosclerosis.
Life Sciences 2007 (2007) Proc Life Sciences, PC484
Poster Communications: Localisation of the chemokine MIP-1β to human arteries and veins
K. L. Jones1, R. E. Kuc1, S. Butler1, C. Holt1, E. J. Mead1, S. D. Katugampola2, J. J. Maguire1, A. P. Davenport1
1. Clinical Pharmacology Unit, University of Cambridge, Cambridge, United Kingdom. 2. Pfizer Global Research and Development, Sandwich, Kent, United Kingdom.
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Where applicable, experiments conform with Society ethical requirements.