Stanford S J, Pepper J R, Mitchell J A
Unit of Critical Care, The Royal Brompton and Harefield N.H.S. Trust, Imperial College School of Medicine, Sydney Street, London SW3 6NP.
Br J Pharmacol. 2000 Mar;129(5):835-8. doi: 10.1038/sj.bjp.0703151.
In addition to their traditional contractile function, vascular smooth muscle cells can be stimulated under inflammatory conditions to release a range of potent biological mediators. Indeed, we and others have shown that human vascular smooth muscle release the colony stimulating factors (CSF) granulocyte macrophage-CSF (GM-CSF) and granulocyte-CSF (G-CSF) as well as large amounts of prostaglandins following the induction of cyclo-oxygenase-2 (COX-2), when stimulated with cytokines. Here we demonstrate, for the first time, that co-induced COX-2 activity simultaneously suppresses GM-CSF release and potentiates G-CSF release by human vascular cells. Moreover, the differential regulation of GM-CSF and G-CSF release by COX-2 was mimicked by the prostacyclin (PGI(2)) mimetic, cicaprost. These observations suggest that PGI(2), released following the induction of COX-2, differentially regulates the release of GM-CSF (suppresses) and G-CSF (potentiates) from human vascular cells.
除了其传统的收缩功能外，血管平滑肌细胞在炎症条件下可被刺激释放一系列强效生物介质。事实上，我们和其他人已经表明，当受到细胞因子刺激时，人血管平滑肌在诱导环氧化酶-2（COX-2）后会释放集落刺激因子（CSF）粒细胞巨噬细胞集落刺激因子（GM-CSF）和粒细胞集落刺激因子（G-CSF）以及大量前列腺素。在此我们首次证明，共同诱导的COX-2活性同时抑制人血管细胞释放GM-CSF并增强G-CSF的释放。此外，COX-2对GM-CSF和G-CSF释放的差异调节可被前列环素（PGI(2)）类似物西卡前列素模拟。这些观察结果表明，COX-2诱导后释放的PGI(2)差异调节人血管细胞中GM-CSF（抑制）和G-CSF（增强）的释放。
