Adiponectin promotes migration activities of endothelial progenitor cells via Cdc42/Rac1

被引:46
作者
Nakamura, Nobuhisa
Naruse, Keiko [1 ,2 ]
Matsuki, Takashi
Hamada, Yoji [3 ]
Nakashima, Eitaro
Kamiya, Hideki
Matsubara, Tatsuaki [2 ]
Enomoto, Atsushi [4 ]
Takahashi, Masahide [4 ]
Oiso, Yutaka
Nakamura, Jiro
机构
[1] Nagoya Univ, Dept Endocrinol & Diabet, Grad Sch Med, Showa Ku, Nagoya, Aichi 4668550, Japan
[2] Aichi Gakuin Univ, Sch Dent, Dept Internal Med, Nagoya, Aichi 464, Japan
[3] Nagoya Univ, Dept Metab Dis, Sch Med, Nagoya, Aichi 4668550, Japan
[4] Nagoya Univ, Dept Pathol, Grad Sch Med, Nagoya, Aichi 4668550, Japan
来源
FEBS LETTERS | 2009年 / 583卷 / 15期
关键词
Adiponectin; Endothelial progenitor cell; Migration; Cdc42; Rac1; TYPE-2; DIABETES-MELLITUS; ACTIVATED PROTEIN-KINASE; INSULIN-RESISTANCE; GLOBULAR ADIPONECTIN; THERAPEUTIC NEOVASCULARIZATION; STIMULATES ANGIOGENESIS; RHO-GTPASES; FOLLOW-UP; NUMBER; AKT;
D O I
10.1016/j.febslet.2009.07.011
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Adiponectin has anti-atherosclerotic effects through its direct actions on vascular cells. The present study investigates the molecular mechanisms of adiponectin in the migration of endothelial progenitor cells (EPCs) which play an important role in neovascularization and re-endothelization. The phosphorylation of Akt and the activations of Cdc42 and Rac1 were significantly increased by adiponectin. Adiponectin increased the migration activity of EPCs, which was completely inhibited by a PI3-kinase inhibitor. siRNA of Cdc42 or Rac1 completely inhibited the adiponectin-induced migration, but siRNA of Akt had no effects, indicating that adiponectin promotes the migration activities of EPCs mainly through PI3-kinase/Cdc42/Rac1.
引用
收藏
页码:2457 / 2463
页数:7
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