Release of GM‐CSF and G‐CSF by human arterial and venous smooth muscle cells: differential regulation by COX‐2

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Abstract
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 (PGI2) mimetic, cicaprost. These observations suggest that PGI2, released following the induction of COX‐2, differentially regulates the release of GM‐CSF (suppresses) and G‐CSF (potentiates) from human vascular cells. British Journal of Pharmacology (2000) 129, 835–838; doi:10.1038/sj.bjp.0703151

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