Angiogenin activates human umbilical artery smooth muscle cells.
Angiogenin stimulates proliferation of human umbilical artery smooth muscle cells. This activity of angiogenin depends on the cell density and requires nuclear translocation of the ligand as well as activation of SAPK/JNK MAP kinase. Angiogenin binds to a 170-kDa putative receptor on the cell surface and induces phosphorylation of SAPK/JNK. It also undergoes nuclear translocation in a time and concentration dependent manner. Neomycin inhibits nuclear translocation of angiogenin and abolishes angiogenin-induced cell proliferation but does not inhibit SAPK/JNK phosphorylation. The data demonstrate that smooth muscle cells are targets for angiogenin and that both SAPK/JNK phosphorylation and nuclear translocation of the ligand are required for angiogenin to activate smooth muscle cells.
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Center for Biochemical and Biophysical Sciences and Medicine, Department of Radiology, Harvard Medical School, 250 Longwood Avenue, Boston, Massachusetts 02115, USA.
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D002452:Cell Count; D002455:Cell Division; D002467:Cell Nucleus / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000187:drug effects*; D009355:Neomycin / Q000494:pharmacology; D011485:Protein Binding; D021381:Protein Transport / Q000187:drug effects; D012259:Ribonuclease, Pancreatic / Q000494:pharmacology*; D014469:Umbilical Arteries / Q000166:cytology*
D020928:Mitogen-Activated Protein Kinases; C046366:angiogenin; D012259:Ribonuclease, Pancreatic; D009355:Neomycin