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Am J Physiol Heart Circ Physiol 279: H2735-H2742, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H2735-H2742, December 2000

Antiproliferative effect of UTP on human arterial and venous smooth muscle cells

Pamela J. White1,2, Rajendra Kumari1,2, Karen E. Porter3, Nicholas J. M. London3, Leong L. Ng4, and Michael R. Boarder1,2

1 Cell Signalling Laboratory, Department of Biological Sciences, De Montfort University, Leicester LE1 9BH; and 2 Department of Cell Physiology and Pharmacology, 3 Department of Surgery, and 4 Department of Medicine and Pharmacology, University of Leicester, Leicester LE1 9HN, United Kingdom

We have investigated the hypothesis that responses associated with proliferation are regulated by extracellular nucleotides such as ATP and UTP in cultured human vascular smooth muscle cells (VSMC) derived from internal mammary artery (IMA) and saphenous vein (SV). Platelet-derived growth factor (PDGF), ATP, and UTP each generated an increase in cytosolic free Ca2+ concentration ([Ca2+]i) in both IMA- and SV-derived cells in the absence of detectable inositol 1,4,5-trisphosphate production. ATP alone had no effect on [3H]thymidine incorporation into DNA, but with a submaximal concentration of PDGF it raised [3H]thymidine incorporation in SV- but not IMA-derived cells. UTP alone also was without effect on [3H]thymidine incorporation or cell number. However, in both SV- and IMA-derived cells, UTP reduced the PDGF-stimulated [3H]thymidine response and PDGF-stimulated cell proliferation. This cannot be explained by an inhibitory effect on the p42/p44 mitogen-activated protein kinase (MAPK) cascade, since this response to PDGF was not attenuated by UTP. We conclude that, in human VSMC of both arterial and venous origin, UTP acts as an anti-proliferative regulator.

vascular smooth muscle; P2Y receptors; P2 receptors; platelet-derived growth factor; cell proliferation


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