Propofol Inhibits Platelet-derived Growth Factor-stimulated Migration in Rat Aortic Smooth Muscle Cells.
10.4097/kjae.2008.54.3.S22
- Author:
Kyuchang LEE
1
;
Keunsang LEE
;
Bokyung KIM
;
Jeongae LIM
;
Jaiwon KOO
;
Myeongjong LEE
;
Hwan Myung LEE
;
Chang Kwon LEE
;
Kyung Jong WON
Author Information
1. Department of Anesthesiology and Pain Medicine, College of Medicine, Konkuk University, Chungju, Korea.
- Publication Type:Original Article
- Keywords:
cofilin;
migration;
propofol;
rat aortic smooth muscle cell
- MeSH:
Acetic Acid;
Animals;
Blotting, Western;
Egtazic Acid;
Emigration and Immigration;
Ethylenes;
Muscle, Smooth;
Muscle, Smooth, Vascular;
Myocytes, Smooth Muscle;
Oxazoles;
Phosphorylation;
Platelet-Derived Growth Factor;
Propofol;
Protein Phosphatase 2;
Protein Tyrosine Phosphatases;
Rats
- From:Korean Journal of Anesthesiology
2008;54(3):S22-S28
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Propofol is the extensively used general anesthetic-sedative agent.Although propofol is known to be involved in migration of various cells, migration response to it in vascular smooth muscle cells is not investigated. This study was carried out to determine the role of propofol in migration of rat aortic smooth muscle cells (RASMCs). METHODS: A7r5 RASMCs were used.Cell migration was examined by the analysis of 5 ng/ml of platelet-derived growth factor (PDGF)-induced RASMC response after treatment of cells with propofol (1-100micrometer) in the Boyden chamber.The activity of cofilin by propofol in RASMCs was measured by the Western blot analysis for the change of cofilin dephosphorylaton in cells treated with 10micrometer propofol for 5, 10, 15 and 20 min, for the effect of propofol (1, 10 and 100micrometer) on cofilin phosphorylation, and for the effects of ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetra acetic acid (2 mM; EGTA), Na3VO4 (200micrometer), and calyculin A (10 nM) on 10micrometer propofol-induced cofilin dephosphorylation. RESULTS: PDGF increased RASMC migration and this response was dose-dependently inhibited by treatment with propofol. Propofol attenuated the cofilin phosphorylation in RASMCs in a dose- and time-dependent manner.Propofol-induced dephosphorylation of cofilin in RASMCs was abolished by calyculin A, a protein phosphatase 2A inhibitor, but not by EGTA, a Ca2+ chelating agent, or Na3VO4, a protein tyrosine phosphatase inhibitor. CONCLUSIONS: The present results suggest that propofol induces the diminution of PDGF-stimulated RASMC migration and this response may be associated with dephosphorylation of cofilin mediated by the protein phosphatase 2A-dependent pathway.
