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Circulation. 2002;105:2893-2898
Published online before print May 20, 2002, doi: 10.1161/01.CIR.0000018622.84402.FF
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(Circulation. 2002;105:2893.)
© 2002 American Heart Association, Inc.

Basic Science Reports

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; Shinji Kihara, MD, PhD; Noriyuki Ouchi, MD, PhD; Kazuhisa Maeda, MD, PhD; Hiroshi Kuriyama, MD, PhD; Yoshihisa Okamoto, MD; Masahiro Kumada, MD; Kikuko Hotta, MD, PhD; Makoto Nishida, MD, PhD; Masahiko Takahashi, MD, PhD; Tadashi Nakamura, MD, PhD; Iichiro Shimomura, MD, PhD; Masahiro Muraguchi, PhD; Yasukazu Ohmoto, PhD; Tohru Funahashi, MD, PhD; Yuji Matsuzawa, MD, PhD

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.

Correspondence to Shinji Kihara, Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2 B5 Yamadaoka, Suita, Osaka 565-0871, Japan. 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 {alpha}-receptor or EGF receptor.

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.


Key Words: atherosclerosis • muscle smooth • growth substances




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