Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / metabolism
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Adiponectin / genetics
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Adiponectin / metabolism*
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Cell Movement / physiology*
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Cells, Cultured
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Endothelial Cells / cytology
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Endothelial Cells / physiology*
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Enzyme Activation
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Female
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Fetal Blood / cytology
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Humans
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Phosphatidylinositol 3-Kinases / genetics
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Phosphatidylinositol 3-Kinases / metabolism
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Phosphorylation
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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RNA, Small Interfering / genetics
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RNA, Small Interfering / metabolism
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Receptors, Adiponectin / metabolism
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Stem Cells / cytology
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Stem Cells / physiology*
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Vascular Endothelial Growth Factor A / metabolism
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cdc42 GTP-Binding Protein / genetics
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cdc42 GTP-Binding Protein / metabolism*
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rac1 GTP-Binding Protein / genetics
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rac1 GTP-Binding Protein / metabolism*
Substances
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ADIPOR1 protein, human
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ADIPOR2 protein, human
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Actins
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Adiponectin
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RNA, Small Interfering
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Receptors, Adiponectin
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Vascular Endothelial Growth Factor A
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Phosphatidylinositol 3-Kinases
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Proto-Oncogene Proteins c-akt
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cdc42 GTP-Binding Protein
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rac1 GTP-Binding Protein