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Am J Physiol Heart Circ Physiol 275: H662-H667, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 2, H662-H667, August 1998

Oncostatin M regulates endothelin-1 production in human endothelial cells

Outi Saijonmaa1,2, Tuulikki Nyman1, Päivi Pacek1,2, and Frej Fyhrquist1,2

1 Minerva Institute for Medical Research and 2 Department of Internal Medicine, Helsinki University Central Hospital, SF-00250 Helsinki, Finland

The effect of the macrophage- and T-lymphocyte-derived cytokine oncostatin M (OSM) on endothelin-1 (ET-1) production in cultured human umbilical cord vein endothelial cells (HUVEC) was studied. OSM (2.5-10 ng/ml) stimulated ET-1 production and the expression of preproendothelin-1 mRNA. The stimulatory effect of OSM was reversed by anti-interleukin (IL)-6 IgG (33 µg/ml). IL-6 (10 ng/ml) was shown to stimulate ET-1 production. The tyrosine kinase inhibitors herbimycin (250-500 ng/ml) and genistein (1-4 µg/ml) suppressed basal ET-1 production and reversed the stimulatory effect of OSM, whereas daidzein (1-8 µg/ml), a less active analog of genistein, had no effect on basal ET-1 production and only partly reversed the stimulatory effect of OSM. The phorbol ester phorbol 12-myristate 13-acetate (PMA) inhibited ET-1 production. Downregulation of protein kinase C (PKC) with PMA (1 µM) preincubation potentiated OSM-induced ET-1 production. In summary, OSM stimulated ET-1 production in cultured HUVEC. The stimulation was probably mediated by IL-6. Furthermore, the present data suggest that tyrosine kinase activation was involved in ET-1 stimulation and that PKC activation leads to suppression of basal and OSM-stimulated ET-1 production.

endothelin-1; human umbilical cord vein endothelial cells; interleukin-6


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