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ETS‐1 converts endothelial cells to the angiogenic phenotype by inducing the expression of matrix metalloproteinases and integrin β 3
Author(s) -
Oda Nobuyuki,
Abe Mayumi,
Sato Yasufumi
Publication year - 1999
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199902)178:2<121::aid-jcp1>3.0.co;2-f
Subject(s) - angiogenesis , vitronectin , matrix metalloproteinase , microbiology and biotechnology , integrin , cell culture , biology , endothelial stem cell , phenotype , chemistry , cancer research , cell , in vitro , gene , genetics
The transcription factor ETS‐1 is induced in endothelial cells (ECs) by angiogenic growth factors and the specific elimination of ETS‐1 synthesis by antisense oligodeoxynucleotide inhibited angiogenesis in vitro (Iwasaka et al., 1996, J Cell Physiol 169:522–531). To understand the precise role of ETS‐1 in angiogenesis, we established both high and low ETS‐1 expression EC lines and compared angiogenic properties of these cell lines with those of the parental murine EC line, MSS‐31. Although growth rate was almost identical for each cell line, the invasiveness was markedly enhanced in high ETS‐1 expression cells and reduced in low ETS‐1 expression cells compared with that of parental cells. The gene expressions of matrix metalloproteinases (MMP‐1, MMP‐3, and MMP‐9) and gelatinolytic activity of MMP‐9 were significantly increased in high ETS‐1 expression cells. Low ETS‐1 expression cells could not spread on a vitronectin substratum, and the phosphorylation of focal adhesion kinase was markedly impaired because of the reduced expression of integrin β 3 . These results indicate that ETS‐1 is a principal regulator that converts ECs to the angiogenic phenotype. J Cell Physiol 178:121–132, 1999. © 1999 Wiley‐Liss, Inc.