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Cyclooxygenase‐2 activity is necessary for the angiogenic properties of oncostatin M
Author(s) -
Pourtau Jérôme,
Mirshahi Farrokh,
Li Hong,
Muraine Marc,
Vincent Loïc,
Tedgui Alain,
Vannier Jean-Pierre,
Soria Jeannette,
Vasse Marc,
Soria Claudine
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01301-0
Subject(s) - oncostatin m , angiogenesis , umbilical vein , cyclooxygenase , leukemia inhibitory factor , cytokine , chemistry , in vivo , endothelial stem cell , interleukin 6 , cancer research , microbiology and biotechnology , in vitro , biology , biochemistry , immunology , enzyme
Macrophages play a major role in angiogenesis. We recently reported that oncostatin M (OSM), a cytokine of the interleukin (IL)‐6 family secreted by macrophages, has a potent angiogenic activity on human microvascular endothelial cells (HMEC‐1), but has no effect on macrovascular cells (human umbilical vein endothelial cells (HUVECs)). In this work, we show that in HMEC‐1, OSM (0.5–2.5 ng/ml), leukemia inhibitory factor (LIF) (25 ng/ml), bFGF (25 ng/ml) and IL‐1β (5 ng/ml) induced production of cyclooxygenase (COX)‐2. In contrast, in HUVECs, neither OSM nor LIF induced COX‐2 mRNA, suggesting that COX‐2 might be implicated in the angiogenic activity of OSM. This was confirmed by the inhibiting effect on OSM‐induced HMEC‐1 proliferation of specific COX‐2 inhibitors. In vivo studies confirmed this findings. We conclude that induction of COX‐2 by OSM is necessary for its angiogenic activity, but is not sufficient since IL‐1β, which also induces COX‐2 in HMEC‐1, has only a poor proliferative effect.