Identification of angiogenic properties of insulin like growth factor II in in vitro angiogenesis models

O. H. Lee, S. K. Bae, M. H. Bae, Y. M. Lee, E. J. Moon, H. J. Cha, Young-Guen Kwon, K. W. Kim

Research output: Contribution to journalArticle

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Abstract

Insulin-like growth factor II (IGF-II), highly expressed in a number of human tumours, has been recently known to promote neovascularization in vivo. Yet, the detailed mechanism by which IGF-II induces angiogenesis has not been well defined. In the present study, we explored an angiogenic activity of IGF-II in in vitro angiogenesis model. Human umbilical vein endothelial cells (HUVECs) treated with IGF-II rapidly aligned and formed a capillary-like network on Matrigel. In chemotaxis assay, IGF-II remarkably increased migration of HUVECs. A rapid and transient activation of p38 mitogen-activated protein kinase (p38 MARK) and p125 focal adhesion kinase (p125(FAK)) phosphorylation was detected in HUVECs exposed to IGF-II. IGF-II also stimulated invasion of HUVECs through a polycarbonate filter coated with Matrigel. Quantitative gelatin-based zymography identified that matrix metalloproteinase-2 (MMP-2) activity generated from HUVECs was increased by IGF-II. This induction of MMP-2 activity was correlated with Northern blot analysis, showing in HUVECs that IGF-II increased the expression of MMP-2 mRNA, while it did not affect that of TIMP-2, a tissue inhibitor of MMP-2. These results provide the evidence that IGF-II directly induces angiogenesis by stimulating migration and morphological differentiation of endothelial cells, and suggest that IGF-II may play a crucial role in the progression of tumorigenesis by promoting the deleterious neovascularization.

Original languageEnglish
Pages (from-to)385-391
Number of pages7
JournalBritish journal of cancer
Volume82
Issue number2
Publication statusPublished - 2000 Jan 25

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Insulin-Like Growth Factor II
Human Umbilical Vein Endothelial Cells
Matrix Metalloproteinase 2
Tissue Inhibitor of Metalloproteinase-2
polycarbonate
In Vitro Techniques
Focal Adhesion Protein-Tyrosine Kinases
p38 Mitogen-Activated Protein Kinases
Chemotaxis
Gelatin
Northern Blotting
Carcinogenesis
Endothelial Cells
Phosphorylation

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Lee, O. H., Bae, S. K., Bae, M. H., Lee, Y. M., Moon, E. J., Cha, H. J., ... Kim, K. W. (2000). Identification of angiogenic properties of insulin like growth factor II in in vitro angiogenesis models. British journal of cancer, 82(2), 385-391.
Lee, O. H. ; Bae, S. K. ; Bae, M. H. ; Lee, Y. M. ; Moon, E. J. ; Cha, H. J. ; Kwon, Young-Guen ; Kim, K. W. / Identification of angiogenic properties of insulin like growth factor II in in vitro angiogenesis models. In: British journal of cancer. 2000 ; Vol. 82, No. 2. pp. 385-391.
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abstract = "Insulin-like growth factor II (IGF-II), highly expressed in a number of human tumours, has been recently known to promote neovascularization in vivo. Yet, the detailed mechanism by which IGF-II induces angiogenesis has not been well defined. In the present study, we explored an angiogenic activity of IGF-II in in vitro angiogenesis model. Human umbilical vein endothelial cells (HUVECs) treated with IGF-II rapidly aligned and formed a capillary-like network on Matrigel. In chemotaxis assay, IGF-II remarkably increased migration of HUVECs. A rapid and transient activation of p38 mitogen-activated protein kinase (p38 MARK) and p125 focal adhesion kinase (p125(FAK)) phosphorylation was detected in HUVECs exposed to IGF-II. IGF-II also stimulated invasion of HUVECs through a polycarbonate filter coated with Matrigel. Quantitative gelatin-based zymography identified that matrix metalloproteinase-2 (MMP-2) activity generated from HUVECs was increased by IGF-II. This induction of MMP-2 activity was correlated with Northern blot analysis, showing in HUVECs that IGF-II increased the expression of MMP-2 mRNA, while it did not affect that of TIMP-2, a tissue inhibitor of MMP-2. These results provide the evidence that IGF-II directly induces angiogenesis by stimulating migration and morphological differentiation of endothelial cells, and suggest that IGF-II may play a crucial role in the progression of tumorigenesis by promoting the deleterious neovascularization.",
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Lee, OH, Bae, SK, Bae, MH, Lee, YM, Moon, EJ, Cha, HJ, Kwon, Y-G & Kim, KW 2000, 'Identification of angiogenic properties of insulin like growth factor II in in vitro angiogenesis models', British journal of cancer, vol. 82, no. 2, pp. 385-391.

Identification of angiogenic properties of insulin like growth factor II in in vitro angiogenesis models. / Lee, O. H.; Bae, S. K.; Bae, M. H.; Lee, Y. M.; Moon, E. J.; Cha, H. J.; Kwon, Young-Guen; Kim, K. W.

In: British journal of cancer, Vol. 82, No. 2, 25.01.2000, p. 385-391.

Research output: Contribution to journalArticle

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AU - Lee, O. H.

AU - Bae, S. K.

AU - Bae, M. H.

AU - Lee, Y. M.

AU - Moon, E. J.

AU - Cha, H. J.

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AU - Kim, K. W.

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N2 - Insulin-like growth factor II (IGF-II), highly expressed in a number of human tumours, has been recently known to promote neovascularization in vivo. Yet, the detailed mechanism by which IGF-II induces angiogenesis has not been well defined. In the present study, we explored an angiogenic activity of IGF-II in in vitro angiogenesis model. Human umbilical vein endothelial cells (HUVECs) treated with IGF-II rapidly aligned and formed a capillary-like network on Matrigel. In chemotaxis assay, IGF-II remarkably increased migration of HUVECs. A rapid and transient activation of p38 mitogen-activated protein kinase (p38 MARK) and p125 focal adhesion kinase (p125(FAK)) phosphorylation was detected in HUVECs exposed to IGF-II. IGF-II also stimulated invasion of HUVECs through a polycarbonate filter coated with Matrigel. Quantitative gelatin-based zymography identified that matrix metalloproteinase-2 (MMP-2) activity generated from HUVECs was increased by IGF-II. This induction of MMP-2 activity was correlated with Northern blot analysis, showing in HUVECs that IGF-II increased the expression of MMP-2 mRNA, while it did not affect that of TIMP-2, a tissue inhibitor of MMP-2. These results provide the evidence that IGF-II directly induces angiogenesis by stimulating migration and morphological differentiation of endothelial cells, and suggest that IGF-II may play a crucial role in the progression of tumorigenesis by promoting the deleterious neovascularization.

AB - Insulin-like growth factor II (IGF-II), highly expressed in a number of human tumours, has been recently known to promote neovascularization in vivo. Yet, the detailed mechanism by which IGF-II induces angiogenesis has not been well defined. In the present study, we explored an angiogenic activity of IGF-II in in vitro angiogenesis model. Human umbilical vein endothelial cells (HUVECs) treated with IGF-II rapidly aligned and formed a capillary-like network on Matrigel. In chemotaxis assay, IGF-II remarkably increased migration of HUVECs. A rapid and transient activation of p38 mitogen-activated protein kinase (p38 MARK) and p125 focal adhesion kinase (p125(FAK)) phosphorylation was detected in HUVECs exposed to IGF-II. IGF-II also stimulated invasion of HUVECs through a polycarbonate filter coated with Matrigel. Quantitative gelatin-based zymography identified that matrix metalloproteinase-2 (MMP-2) activity generated from HUVECs was increased by IGF-II. This induction of MMP-2 activity was correlated with Northern blot analysis, showing in HUVECs that IGF-II increased the expression of MMP-2 mRNA, while it did not affect that of TIMP-2, a tissue inhibitor of MMP-2. These results provide the evidence that IGF-II directly induces angiogenesis by stimulating migration and morphological differentiation of endothelial cells, and suggest that IGF-II may play a crucial role in the progression of tumorigenesis by promoting the deleterious neovascularization.

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