IGF-1 Regulates Migration and Angiogenesis of Human Endothelial Cells.

Accession number;99A0391894
Title;IGF-1 Regulates Migration and Angiogenesis of Human Endothelial Cells.
Author; SHIGEMATSU S (Shinshu Univ., Matsumoto, Jpn) YAMAUCHI K (Shinshu Univ., Matsumoto, Jpn) NAKAJIMA K (Shinshu Univ., Matsumoto, Jpn) IIJIMA S (Shinshu Univ., Matsumoto, Jpn) AIZAWA T (Shinshu Univ., Matsumoto, Jpn) HASHIZUME K (Shinshu Univ., Matsumoto, Jpn)
Journal Title;Endocr J
Journal Code:F0625A
ISSN:0918-8959
VOL.46;NO.Supplement;PAGE.S59-S62(1999)
Figure&Table&Reference;FIG.5, REF.2
Pub. Country;Japan
Language;English
Abstract;Recent studies revealed favorable para- and/or autocrine effects of IGF-1 in the pathogenesis of diabetic complications. On the other hand, hyperglycemia is a risk factor for the development of diabetic vascular complications. In this study we examined the effects of high glucose and/or IGF-1 on cell migration and angiogenesis (tubular formation) by using human endothelial cells (EC) in vitro. First we examined cell migration by the two-chamber method. Chronic treatment with a high concentration of D-glucose strongly stimulated the cell migration, which was mimicked by PMA, a protein kinase C (PKC) agonist. The cell migration was also induced by IGF-1. The glucose-induced cell migration was blocked by PKC inhibitor, H7. IGF-1-induced cell migration was not blocked by PD98059, MAPK/ERK kinase (MEK) inhibitor or wortmannin, a phosphatidylinositol (PI) 3-kinase inhibitor. Next we examined the effects of high glucose and/or IGF-1 on the tubular formation of EC. The tubular formation was induced only when the cells were exposed to a combination of high glucose and IGF-1. The tubular formation was blocked by MEK inhibitor and PI 3-kinase inhibitor but not by PKC inhibitor. These results indicate that hyperglycemia and IGF-1, respectively, stimulate the EC migration, and tubular formation is induced by a combination of IGF-1 and hyperglycemia. (author abst.)
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