on May 20, 2002
Circulation. 2002
Published online before print May 20, 2002, doi: 10.1161/01.CIR.0000018622.84402.FF
Published online before print May 20, 2002, doi: 10.1161/01.CIR.0000018622.84402.FF
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Submitted on January 21, 2002
From the Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research (M.M., Y. Ohmoto), Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan. * To whom correspondence should be addressed. E-mail: kihara{at}imed2.med.osaka-u.ac.jp.
Background—Vascular smooth muscle cell proliferation plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the human injured artery and suppressed endothelial inflammatory response as well as macrophage-to-foam cell transformation. The present study investigated the effects of adiponectin on proliferation and migration of human aortic smooth muscle cells (HASMCs). Methods and Results—HASMC proliferation was estimated by [3H] thymidine uptake and cell number. Cell migration assay was performed using a Boyden chamber. Physiological concentrations of adiponectin significantly suppressed both proliferation and migration of HASMCs stimulated with platelet-derived growth factor (PDGF)-BB. Adiponectin specifically bound to 125I-PDGF-BB and significantly inhibited the association of 125I-PDGF-BB with HASMCs, but no effects were observed on the binding of 125I-PDGF-AA or 125I-heparin--binding epidermal growth factor (EGF)--like growth factor (HB-EGF) to HASMCs. Adiponectin strongly and dose-dependently suppressed PDGF-BB--induced p42/44 extracellular signal--related kinase (ERK) phosphorylation and PDGF ß-receptor autophosphorylation analyzed by immunoblot. Adiponectin also reduced PDGF-AA--stimulated or HB-EGF--stimulated ERK phosphorylation in a dose-dependent manner without affecting autophosphorylation of PDGF Conclusions—The adipocyte-derived plasma protein adiponectin strongly suppressed HASMC proliferation and migration through direct binding with PDGF-BB and generally inhibited growth factor--stimulated ERK signal in HASMCs, suggesting that adiponectin acts as a modulator for vascular remodeling.
Revised on April 3, 2002
Accepted on April 3, 2002
Adipocyte-Derived Plasma Protein Adiponectin Acts as a Platelet-Derived Growth Factor-BB--Binding Protein and Regulates Growth Factor--Induced Common Postreceptor Signal in Vascular Smooth Muscle Cell
Yukio Arita MD, PhD,
-receptor or EGF receptor.
Key words: atherosclerosis • muscle smooth • growth substances
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