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Am J Physiol Lung Cell Mol Physiol 288: L1040-L1048, 2005. First published January 21, 2005; doi:10.1152/ajplung.00333.2004
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Oncostatin M causes VEGF release from human airway smooth muscle: synergy with IL-1{beta}

Débora S. Faffe,1,2 Lesley Flynt,1 Matthew Mellema,1 Timothy R. Whitehead,1 Kerri Bourgeois,1 Reynold A. Panettieri, Jr.,3 Eric S. Silverman,1 and Stephanie A. Shore1

1Physiology Program, Harvard School of Public Health, Boston, Massachusetts; 2Laboratory of Respiration Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; and 3Pulmonary and Critical Care Division, Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Submitted 7 September 2004 ; accepted in final form 18 January 2005

Vascular endothelial growth factor (VEGF), a potent angiogenesis factor, likely contributes to airway remodeling in asthma. We sought to examine the effects and mechanism of action of IL-6 family cytokines on VEGF release from human airway smooth muscle (HASM) cells. Oncostatin M (OSM), but not other IL-6 family cytokines, increased VEGF release, and IL-1{beta} enhanced OSM-induced VEGF release. OSM increased VEGF mRNA expression and VEGF promoter activity, whereas IL-1{beta} had no effect. IL-1{beta} did not augment the effects of OSM on VEGF promoter activity but did augment OSM-induced VEGF mRNA expression and mRNA stability. The STAT3 inhibitor piceatannol decreased both OSM-induced VEGF release and synergy between OSM and IL-1{beta}, without affecting responses to IL-1{beta} alone. Piceatannol also inhibited OSM-induced VEGF mRNA expression. In contrast, inhibitors of MAPK pathway had no effect on OSM or OSM plus IL-1{beta}-induced VEGF release. OSM increased type 1 IL-1 receptor (IL-1R1) mRNA expression, as measured by real-time PCR, and piceatannol attenuated this response. Consistent with the increase in IL-1R1 expression, OSM markedly augmented IL-1{beta}-induced VEGF, MCP-1, and IL-6 release. In summary, our data indicate OSM causes VEGF expression in HASM cells by a transcriptional mechanism involving STAT3. IL-1{beta} also synergizes with OSM to increase VEGF release, likely as a result of effects of IL-1{beta} on VEGF mRNA stability as well as effects of OSM on IL-1R1 expression. This is the first description of a role for OSM on IL-1R1 expression in any cell type. OSM may contribute to airway remodeling observed in chronic airway disease.

interleukin-6; interleukin-1 receptor 1; signal transducer and activator of transcription 3; monocyte chemoattractant protein-1; piceatannol; vascular endothelial growth factor


Address for reprint requests and other correspondence: S. Shore, Physiology Program, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115 (E-mail: sshore{at}hsph.harvard.edu)




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