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.

Angiogenin activates human umbilical artery smooth muscle cells / Xu, Z; Monti, DARIA MARIA; Hu, G.. - In: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. - ISSN 0006-291X. - ELETTRONICO. - (2001), pp. 909-914.

Angiogenin activates human umbilical artery smooth muscle cells

MONTI, DARIA MARIA;
2001

Abstract

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.
2001
Angiogenin activates human umbilical artery smooth muscle cells / Xu, Z; Monti, DARIA MARIA; Hu, G.. - In: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. - ISSN 0006-291X. - ELETTRONICO. - (2001), pp. 909-914.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/304802
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