Abstract

Background TRPC-mediated Ca entry has been implicated in the control of smooth muscle proliferation and might represent a pivotal mechanism underlying in-stent restenosis. As we have observed significant expression of TRPC3 in human smooth muscle from coronary arteries as well as from aorta, we tested the efficiency of a recently discovered TRPC3-selective Ca entry blocker, Pyr3 (10 μM) to prevent vascular smooth muscle proliferation and stent implantation-induced hyperplasia of human aorta.

Highlights

  • TRPC-mediated Ca2+ entry has been implicated in the control of smooth muscle proliferation and might represent a pivotal mechanism underlying in-stent restenosis

  • The effect of Pyr3 on proliferation was measured by detection of BrDU incorporation and PCNA expression in human coronary smooth muscle and microvascular endothelium, which displays significantly smaller expression levels of TRPC as compared to smooth muscle

  • Inhibitory effects of Pyr3 on stent implantation-induced arterial injury were tested using a novel in vitro model of in-stent hyperplasia in human arteries based on organ-typical culture of human aortic constructs

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Summary

Open Access

Sarah König1, Sara Browne1, Heinrich Mächler2, Gerald Höfler3, C Oliver Kappe4, Toma N Glasnov4, Marlen Braune5, Eric Wittchow5, Klaus Groschner1* From 18th Scientific Symposium of the Austrian Pharmacological Society (APHAR). Joint meeting with the Croatian, Serbian and Slovenian Pharmacological Societies. Graz, Austria. 20-21 September 2012

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