Catechins inhibit angiotensin II-induced vascular smooth muscle cell proliferation via mitogen-activated protein kinase pathway.
- Author:
Sun Mi WON
1
;
Youn Hee PARK
;
Hee Jung KIM
;
Kwon Moo PARK
;
Won Jung LEE
Author Information
1. Department of Physiology, School of Medicine, Kyungpook National University, Daegu, Korea. wjleek@knu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
angiotensin II;
catechin;
mitogen-activated protein kinase;
muscle, smooth, vascular;
proto-oncogene proteins c-fos;
proto-oncogene proteins c-jun
- MeSH:
Signal Transduction/drug effects;
Rats, Sprague-Dawley;
Rats;
RNA, Messenger/metabolism;
Proto-Oncogene Proteins c-jun/metabolism;
Proto-Oncogene Proteins c-fos/metabolism;
Phosphorylation;
Nucleic Acid Synthesis Inhibitors/pharmacology;
Muscle, Smooth, Vascular/cytology/*drug effects;
Mitogen-Activated Protein Kinases/*metabolism/physiology;
Female;
DNA/biosynthesis;
Cells, Cultured;
Cell Proliferation/*drug effects;
Cell Culture Techniques;
Catechin/analogs & derivatives/*pharmacology/physiology;
Animals;
Angiotensin II/*pharmacology
- From:Experimental & Molecular Medicine
2006;38(5):525-534
- CountryRepublic of Korea
- Language:English
-
Abstract:
Catechins, components of green tea, reduce the incidence of cardiovascular diseases such as atherosclerosis. Angiotensin II (Ang II) is highly implicated in the proliferation of vascular smooth muscle cells (VSMC), resulting in atherosclerosis. The acting mechanisms of the catechins remain to be defined in the proliferation of VSMC induced by Ang II. Here we report that catechin, epicatechin (EC), epicatechingallate (ECG) or epigallocatechingallate (EGCG) significantly inhibits the Ang II-induced [3H]thymidine incorporation into the primary cultured rat aortic VSMC. Ang II increases the phosphorylation of the extracellular signal-regulated protein kinase 1/2 (ERK 1/2), c-jun-N-terminal kinase 1/2 (JNK 1/2), or p38 mitogen-activated protein kinases (MAPKs) and mRNA expression of c-jun and c-fos. The EGCG pretreatment inhibits the Ang II-induced phosphorylation of ERK 1/2, JNK 1/2, or p38 MAPK, and the expression of c-jun or c-fos mRNA. U0126, a MEK inhibitor, SP600125, a JNK inhibitor, or SB203580, a p38 inhibitor, attenuates the Ang II-induced [3H]thymidine incorporation into the VSMC. In conclusion, catechins inhibit the Ang II-stimulated VSMC proliferation via the inhibition of the Ang II-stimulated activation of MAPK and activator protein-1 signaling pathways. The antiproliferative effect of catechins may be associated with the reduced risk of cardiovascular diseases by the intake of green tea. Catechins may be useful in the development of prevention and therapeutics of vascular diseases.
