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Involvement of interleukin‐1β‐converting enzyme in apoptosis of bFGF‐deprived murine aortic endothelial cells
Author(s) -
Kondo Seiji,
Kondo Yasuko,
Yin Dali,
Barnett Gene H.,
Kaakaji Rami,
Peterson John W.,
Mormura Tatsuo,
Kubo Hiroaki,
Takeuchi Juji,
Barna Barbara P.
Publication year - 1996
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.10.10.8751721
Subject(s) - apoptosis , microbiology and biotechnology , basic fibroblast growth factor , programmed cell death , endothelial stem cell , biology , chemistry , growth factor , biochemistry , in vitro , receptor
Apoptosis (programmed cell death) is an essential physiological process that is genetically regulated and contributes to the balance between cell growth, differentiation, and the maintenance of normal cells. Recent studies show that deprivation of growth factor induces apoptosis in endothelial cells. However, the molecular mechanisms regulating apoptosis remain unclear. In this study, we demonstrate that deprivation of basic fibroblast growth factor (bFGF) increased the expression of interleukin‐1β‐converting enzyme (ICE) protein, and subsequently induced apoptosis in murine aortic endothelial (MAE) cells. In contrast, the proteins of the tumor suppressor p53 and c‐myc were undetected during apoptosis. This apoptosis was suppressed by the tetrapeptide ICE inhibitor, Ac‐YVAD‐CMK. Overexpression of murine ICE, in addition, induced apoptosis in MAE cells using gene transfer techniques. These results strongly suggest that ICE may mediate apoptosis in bFGF‐deprived endothelial cells, and the suppression of ICE function could represent a novel approach for the protection of endothelial cells from damages.—Kondo, S., Kondo, Y., Yin, D., Barnett, G. H., Kaakaji, R., Peterson, J. W., Morimura, T., Kubo, H., Takeuchi, J., Barna, B. P. Involvement of interleukin‐1β converting enzyme in apoptosis of bFGF‐deprived murine aortic endothelial cells. FASEB J. 10, 1192‐1197 (1996)