Published online before print January 26, 2006, doi: 10.1161/01.RES.0000204724.29685.db
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© 2006 American Heart Association, Inc.
Integrative Physiology |
Upregulated TRPC1 Channel in Vascular Injury In Vivo and Its Role in Human Neointimal Hyperplasia
From the Institute of Membrane & Systems Biology (B.K., S.S.S., A.C., S.-Z.X., P.S., J.N., D.M., D.J.B.) and Cardiovascular Research Institute (K.E.P.), University of Leeds, United Kingdom; Yorkshire Heart Centre (B.K., S.S.S., C.M.M.), General Infirmary at Leeds, United Kingdom; Department of Experimental Medical Science (K.D., A.B., A.H.-N., M.F.G., P.H.), Biomedical Centre, Lund University, Sweden; Excellence Research Centre for Cardiovascular Diseases (A.F., M.C.), Department of Experimental Medicine, Second University of Naples, Italy; and School of Medicine (P.A.K., A.M.H.), University of Manchester, United Kingdom.
Correspondence to Prof David J Beech, Institute of Membrane & Systems Biology, Garstang Building, University of Leeds, Leeds, LS2 9JT, England, United Kingdom. E-mail d.j.beech{at}leeds.ac.uk
Occlusive vascular disease is a widespread abnormality leading to lethal or debilitating outcomes such as myocardial infarction and stroke. It is part of atherosclerosis and is evoked by clinical procedures including angioplasty and grafting of saphenous vein in bypass surgery. A causative factor is the switch in smooth muscle cells to an invasive and proliferative mode, leading to neointimal hyperplasia. Here we reveal the importance to this process of TRPC1, a homolog of Drosophila transient receptor potential. Using 2 different in vivo models of vascular injury in rodents we show hyperplasic smooth muscle cells have upregulated TRPC1 associated with enhanced calcium entry and cell cycle activity. Neointimal smooth muscle cells after balloon angioplasty of pig coronary artery also express TRPC1. Furthermore, human vein samples obtained during coronary artery bypass graft surgery commonly exhibit an intimal structure containing smooth muscle cells that expressed more TRPC1 than the medial layer cells. Veins were organ cultured to allow growth of neointimal smooth muscle cells over a 2-week period. To explore the functional relevance of TRPC1, we used a specific E3-targeted antibody to TRPC1 and chemical blocker 2-aminoethoxydiphenyl borate. Both agents significantly reduced neointimal growth in human vein, as well as calcium entry and proliferation of smooth muscle cells in culture. The data suggest upregulated TRPC1 is a general feature of smooth muscle cells in occlusive vascular disease and that TRPC1 inhibitors have potential as protective agents against human vascular failure.
Key Words: neointimal hyperplasia • vascular smooth muscle cells • calcium channel • transient receptor potential
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