Cilostazol Inhibits Vascular Smooth Muscle Cell Proliferation and Reactive Oxygen Species Production through Activation of AMP-activated Protein Kinase Induced by Heme Oxygenase-1

Title
Cilostazol Inhibits Vascular Smooth Muscle Cell Proliferation and Reactive Oxygen Species Production through Activation of AMP-activated Protein Kinase Induced by Heme Oxygenase-1
Author(s)
최형철김정은성진영우창훈강영진이광윤김희선권우형
Keywords
FATTY-ACID OXIDATION; THERAPEUTIC TARGET; HYPERTENSIVE-RATS; GLUCOSE-UPTAKE; GROWTH; DISEASE; ADIPONECTIN; EXPRESSION; SYSTEM; GENE
Issue Date
201108
Publisher
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
Citation
KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, v.15, no.4, pp.203 - 210
Abstract
Cilostazol is a selective inhibitor of phosphodiesterase 3 that increases intracellular CAMP levels and activates protein kinase A, thereby inhibiting vascular smooth muscle cell (VSMC) proliferation. We investigated whether AMP-activated protein kinase (AMPK) activation induced by heme oxygenase-1 (HO-1) is a mediator of the beneficial effects of cilostazol and whether cilostazol may prevent cell proliferation and reactive oxygen species (ROS) production by activating AMPK in VSMC. In the present study, we investigated VSMC with various concentrations of cilostazol. Treatment with cilostazol increased HO-1 expression and phosphorylation of AMPK in a dose- and time-dependent manner. Cilostazol also significantly decreased platelet-derived growth factor (PDGF)-induced VSMC proliferation and ROS production by activating AMPK induced by HO-1. Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production.
URI
http://hdl.handle.net/YU.REPOSITORY/24812http://dx.doi.org/10.4196/kjpp.2011.15.4.203
ISSN
1226-4512
Appears in Collections:
의과대학 > 약리학교실 > Articles
의과대학 > 미생물학교실 > Articles
의과대학 > 성형외과학교실 > Articles
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