Endothelial cells undergo apoptosis after withdrawal of growth factors, alterations in the extracellular matrix, or exposure to cytokines. Here we report that tumor necrosis factor (TNF)-alpha induces apoptosis of human endothelial cells derived from the umbilical vein in a dose-dependent fashion. Apoptosis is triggered through a pathway that is independent from the levels of Bcl-2. On the contrary, TNF stimulates the growth of spontaneously transformed human umbilical vein endothelial cells. This proliferative effect is mediated through the up-regulation of fibroblast growth factor-1 by TNF. The addition of specific fibroblast growth factor-1 antisense oligonucleotides inhibits TNF-induced fibroblast growth factor-1 expression, thus inhibiting the growth and triggering apoptosis of spontaneously transformed human umbilical vein endothelial cells.
Tumor-necrosis-factor-induced fibroblast growth factor-1 acts as a survival factor in a transformed endothelial cell line / J. A. Maier, D. Morelli, S. Ménard, M. I. Colnaghi, A. Balsari. - In: THE AMERICAN JOURNAL OF PATHOLOGY. - ISSN 0002-9440. - 149:3(1996 Sep), pp. 945-952.
Tumor-necrosis-factor-induced fibroblast growth factor-1 acts as a survival factor in a transformed endothelial cell line
J.A. MaierPrimo
;A. BalsariUltimo
1996
Abstract
Endothelial cells undergo apoptosis after withdrawal of growth factors, alterations in the extracellular matrix, or exposure to cytokines. Here we report that tumor necrosis factor (TNF)-alpha induces apoptosis of human endothelial cells derived from the umbilical vein in a dose-dependent fashion. Apoptosis is triggered through a pathway that is independent from the levels of Bcl-2. On the contrary, TNF stimulates the growth of spontaneously transformed human umbilical vein endothelial cells. This proliferative effect is mediated through the up-regulation of fibroblast growth factor-1 by TNF. The addition of specific fibroblast growth factor-1 antisense oligonucleotides inhibits TNF-induced fibroblast growth factor-1 expression, thus inhibiting the growth and triggering apoptosis of spontaneously transformed human umbilical vein endothelial cells.Pubblicazioni consigliate
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