Selective Inhibitory Effect of Epigallocatechin-3-gallate on Migration of Vascular Smooth Muscle Cells

Molecules

Dong-Wook Han¹  Mi Hee Lee¹  Byeong-Ju Kwon¹  Hye-Lee Kim¹  Suong-Hyu Hyon¹ 

[1]¹Department of Nanomedical Engineering, College of Nanoscience & Nanotechnology, Pusan National University, Busan 609-735, Korea

关键词: eigallocatechin-3-gallate;    vascular endothelial cells;    vascular smooth muscle cells;    proliferation;    migration;   

DOI  :  10.3390/molecules15118488

来源: mdpi

【 摘 要 】

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 mM and VSMCs, 1050 mM). 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 mM 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.

【 授权许可】

CC BY   
This is an open access article distributed under the Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.