Inhibitory effect of Hsp70 on angiotensin II-induced vascular smooth muscle cell hypertrophy
Experimental & Molecular Medicine
;
: 509-518, 2006.
Article
in English
| WPRIM
| ID: wpr-69447
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).
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Aorta
/
Flavonoids
/
Enzyme Stability
/
Angiotensin II
/
Cells, Cultured
/
Protein Tyrosine Phosphatases
/
Rats, Sprague-Dawley
/
Immediate-Early Proteins
/
Phosphoprotein Phosphatases
/
HSP70 Heat-Shock Proteins
Limits:
Animals
Language:
English
Journal:
Experimental & Molecular Medicine
Year:
2006
Type:
Article
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