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This Article Full Text Full Text (PDF) All Versions of this Article: 286/3/H902    most recent 00130.2003v2 00130.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Curcio, A. Articles by Indolfi, C. Search for Related Content PubMed PubMed Citation Articles by Curcio, A. Articles by Indolfi, C.

Effect of stent coating alone on in vitro vascular smooth muscle cell proliferation and apoptosis

¹Division of Cardiology, Department of Experimental and Clinical Medicine, Magna Graecia University, 88100 Catanzaro; ²Division of Cardiology, Federico II University, 80131 Naples; ³Genecor Foundation, Naples; and ⁴Department of Experimental and Clinical Medicine, Magna Graecia University, 88100 Catanzaro, Italy

Submitted 30 July 2003 ; accepted in final form 22 October 2003

Synthetic polymers, like methacrylate (MA) compounds, have been clinically introduced as inert coatings to locally deliver drugs that inhibit restenosis after stent. The aim of the present study was to evaluate the effects of MA coating alone on vascular smooth muscle cell (VSMC) growth in vitro. Stainless steel stents were coated with MA at the following doses: 0.3, 1.5, and 3 ml. Uncoated/bare metal stents were used as controls. VSMCs were cultured in dishes, and a MA-coated stent or an uncoated bare metal stent was gently added to each well. VSMC proliferation was assessed by bromodeoxyuridine (BrdU) incorporation. Apoptosis was analyzed by three distinct approaches: 1) annexin V/propidium iodide fluorescence detection; 2) DNA laddering; and 3) caspase-3 activation and PARP cleavage. MA-coated stents induced a significant decrease of BrdU incorporation compared with uncoated stents at both the low and high concentrations. In VSMCs incubated with MA-coated stents, annexin V/propidium iodide fluorescence detection showed a significant increase in apoptotic cells, which was corroborated by the typical DNA laddering. Apoptosis of VSMCs after incubation with MA-coated stents was characterized by caspase-3 activation and PARP cleavage. The MA-coated stent induced VSMC growth arrest by inducing apoptosis in a dose-dependent manner. Thus MA is not an inert platform for eluting drugs because it is biologically active per se. This effect should be taken in account when evaluating an association of this coating with antiproliferative agents for in-stent restenosis prevention.

restenosis; stents