Inhibitory effect of Hsp70 on angiotensin II-induced vascular smooth muscle cell hypertrophy.
- Author:
Ying ZHENG
1
;
Chang Nim IM
;
Jeong Sun SEO
Author Information
1. ILCHUN Molecular Medicine Institute, Seoul National University College of Medicine, Seoul, Korea. jeongsun@snu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
angiotensin II;
heat shock protein 70;
hypertrophy;
mitogen-activated protein kinases;
muscle, smooth, vascular
- MeSH:
Rats, Sprague-Dawley;
Rats;
RNA, Small Interfering/pharmacology;
Protein-Tyrosine-Phosphatase/metabolism/physiology;
Phosphoprotein Phosphatase/metabolism/physiology;
Muscle, Smooth, Vascular/*cytology/*drug effects;
Mitogen-Activated Protein Kinase 3/antagonists & inhibitors;
Mitogen-Activated Protein Kinase 1/antagonists & inhibitors;
Male;
MAP Kinase Kinase 2/metabolism;
MAP Kinase Kinase 1/metabolism;
Immediate-Early Proteins/metabolism/physiology;
Hypertrophy;
HSP70 Heat-Shock Proteins/antagonists & inhibitors/*pharmacology;
Flavonoids/pharmacology;
Enzyme Stability/drug effects;
Cells, Cultured;
Cell Cycle Proteins/metabolism/physiology;
Aorta/drug effects/pathology;
Animals;
Angiotensin II/*pharmacology
- From:Experimental & Molecular Medicine
2006;38(5):509-518
- CountryRepublic of Korea
- Language:English
-
Abstract:
Angiotensin II (Ang II), which is an important mediator of both vascular responsiveness and growth, has been shown to induce vascular smooth muscle cell (VSMC) hypertrophy via the activation of a complex series of intracellular signaling events. Heat shock protein 70 (Hsp70) has recently been shown to protect against Ang II-induced hypertension. In this study, we tested the hypothesis that Hsp70 can protect VSMC from Ang II-induced hypertrophy. We treated VSMCs with Ang II to induce hypertrophy and to activate MAPK signaling pathway. We observed that the augmentation of Hsp70 expression inhibited Ang II-stimulated VSMC hypertrophy. This inhibitory effect of Hsp70 appears to be partly due to extracellular signal-regulated kinase (ERK1/2) inactivation, which in turn, may possibly result from the accumulation of MAP kinase phosphatase-1 (MKP-1).
