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首页> 外文期刊>American Journal of Physiology >Oncostatin M causes VEGF release from human airway smooth muscle: synergy with IL-1beta.
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Oncostatin M causes VEGF release from human airway smooth muscle: synergy with IL-1beta.

机译：抑癌素M导致VEGF从人气道平滑肌释放：与IL-1beta协同作用。

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摘要

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-1beta enhanced OSM-induced VEGF release. OSM increased VEGF mRNA expression and VEGF promoter activity, whereas IL-1beta had no effect. IL-1beta 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-1beta, without affecting responses to IL-1beta alone. Piceatannol also inhibited OSM-induced VEGF mRNA expression. In contrast, inhibitors of MAPK pathway had no effect on OSM or OSM plus IL-1beta-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-1beta-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-1beta also synergizes with OSM to increase VEGF release, likely as a result of effects of IL-1beta 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.
机译：血管内皮生长因子（VEGF）是有效的血管生成因子，可能有助于哮喘的气道重塑。我们试图检查IL-6家族细胞因子对人呼吸道平滑肌（HASM）细胞释放VEGF的作用和作用机理。抑瘤素M（OSM）而非其他IL-6家族细胞因子可增加VEGF的释放，而IL-1beta则可增强OSM诱导的VEGF的释放。 OSM增加VEGF mRNA表达和VEGF启动子活性，而IL-1beta没有作用。 IL-1beta不会增加OSM对VEGF启动子活性的影响，但会增加OSM诱导的VEGF mRNA表达和mRNA稳定性。 STAT3抑制剂piceatannol降低了OSM诱导的VEGF释放以及OSM与IL-1beta之间的协同作用，但不影响对单独的IL-1beta的反应。 Piceatannol还抑制OSM诱导的VEGF mRNA表达。相反，MAPK途径的抑制剂对OSM或OSM加IL-1beta诱导的VEGF释放没有影响。 OSM增加了1型IL-1受体（IL-1R1）mRNA的表达，这是通过实时PCR测得的，而皮卡汀醇减弱了这种反应。与IL-1R1表达的增加一致，OSM显着增加了IL-1β诱导的VEGF，MCP-1和IL-6的释放。总之，我们的数据表明OSM通过涉及STAT3的转录机制在HASM细胞中引起VEGF表达。 IL-1beta还与OSM协同作用以增加VEGF的释放，这可能是由于IL-1beta对VEGF mRNA稳定性的影响以及OSM对IL-1R1表达的影响所致。这是OSM在任何细胞类型中对IL-1R1表达的作用的第一个描述。 OSM可能有助于慢性气道疾病中观察到的气道重塑。

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