Document Detail

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.
MedLine Citation:
PMID:  12070119     Owner:  NLM     Status:  MEDLINE    
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 [(3)H] 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 (125)I-PDGF-BB and significantly inhibited the association of (125)I-PDGF-BB with HASMCs, but no effects were observed on the binding of (125)I-PDGF-AA or (125)I-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 beta-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.
Yukio Arita; Shinji Kihara; Noriyuki Ouchi; Kazuhisa Maeda; Hiroshi Kuriyama; Yoshihisa Okamoto; Masahiro Kumada; Kikuko Hotta; Makoto Nishida; Masahiko Takahashi; Tadashi Nakamura; Iichiro Shimomura; Masahiro Muraguchi; Yasukazu Ohmoto; Tohru Funahashi; Yuji Matsuzawa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  105     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-06-18     Completed Date:  2002-06-28     Revised Date:  2013-05-20    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2893-8     Citation Subset:  AIM; IM    
Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka and First Institute of New Drug Research, Otsuka Pharmaceutical Co, Ltd, Tokushima, Japan.
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MeSH Terms
Adipocytes / chemistry
Aorta / cytology
Blood Proteins / metabolism,  pharmacology
Cell Division
Cell Movement
Cells, Cultured
Dose-Response Relationship, Drug
Growth Inhibitors / metabolism,  pharmacology*
Growth Substances / pharmacology
Intercellular Signaling Peptides and Proteins*
Mitogen-Activated Protein Kinases / metabolism
Muscle, Smooth, Vascular / drug effects,  metabolism*,  physiology
Platelet-Derived Growth Factor / antagonists & inhibitors*,  metabolism
Proteins / metabolism,  pharmacology*
Proto-Oncogene Proteins c-sis
Receptors, Growth Factor / antagonists & inhibitors*,  metabolism
Signal Transduction / drug effects
Reg. No./Substance:
0/Adiponectin; 0/Blood Proteins; 0/Growth Inhibitors; 0/Growth Substances; 0/Intercellular Signaling Peptides and Proteins; 0/Platelet-Derived Growth Factor; 0/Proteins; 0/Proto-Oncogene Proteins c-sis; 0/Receptors, Growth Factor; 0/platelet-derived growth factor BB; EC Protein Kinases

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