Abstract
In order to prevent restenosis after angioplasty or stenting, one of the most popular targets is suppression of the abnormal growth and excess migration of vascular smooth muscle cells (VSMCs) with drugs. However, the drugs also adversely affect vascular endothelial cells (VECs), leading to the induction of late thrombosis. We have investigated the effect of epigallocatechin-3-gallate (EGCG) on the proliferation and migration of VECs and VSMCs. Both cells showed dose-dependent decrease of viability in response to EGCG while they have different IC50 values of EGCG (VECs, 150 μM and VSMCs, 1050 μM). Incubating both cells with EGCG resulted in significant reduction in cell proliferation irrespective of cell type. The proliferation of VECs were greater affected than that of VSMCs at the same concentrations of EGCG. EGCG exerted differential migration-inhibitory activity in VECs vs. VSMCs. The migration of VECs was not attenuated by 200 μM EGCG, but that of VSMCs was significantly inhibited at the same concentration of EGCG. It is suggested that that EGCG can be effectively used as an efficient drug for vascular diseases or stents due to its selective activity, completely suppressing the proliferation and migration of VSMCs, but not adversely affecting VECs migration in blood vessels.
Highlights
Intimal hyperplasia leading to restenosis is the major process that limits the success of cardiovascular intervention
Direct injury to vascular cells is an important stimulus for the production of autocrine-paracrine growth factors, such as PDGF-AA, TGF- 1, basic fibroblast growth factor and insulin-like growth factor I, that promote the proliferation of vascular smooth muscle cells (VSMCs), whereas blood-borne factors (e.g., PDGF-BB and thrombin) appear to be more important in promoting the migration of VSMCs into the subintimal space [3,4,5]
We investigated the effect of EGCG on the cellular behaviors of vascular cells, endothelial cell (EC) and SMCs they were originated from different species, i.e. human and rat, respectively
Summary
Intimal hyperplasia leading to restenosis is the major process that limits the success of cardiovascular intervention. Neointimal hyperplasia in response to arterial injury is a complex process, classically believed to be the consequence of vascular smooth muscle cell (VSMC) proliferation and migration, and the synthesis of extracellular matrix [1]. Mechanisms that have been suggested as being involved in the antiatherosclerotic effects of green tea consumption primarily entail antioxidative, anti-inflammatory, antiproliferative and antithrombotic properties, as well as beneficial effects on endothelial function [13,14,15]. Many in vitro and in vivo studies have shown that green tea polyphenolic compounds (GTPCs) has potent antioxidative, radical-scavenging metal ions-chelating, and redox-sensitive transcription factors-inhibiting properties, which may partially account for their antiatherogenic effects [15,16,17].
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