INDUCTION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR EXPRESSION IN SYNOVIAL FIBROBLASTS BY PROSTAGLANDIN-E AND INTERLEUKIN-1 - A POTENTIAL MECHANISM FOR INFLAMMATORY ANGIOGENESIS
INDUCTION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR EXPRESSION IN SYNOVIAL FIBROBLASTS BY PROSTAGLANDIN-E AND INTERLEUKIN-1 - A POTENTIAL MECHANISM FOR INFLAMMATORY ANGIOGENESIS
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DOI：
10.1016/0014-5793(95)00956-a
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发表时间：
1995-09-18
期刊：
影响因子：
3.5
通讯作者：
HLA, T
中科院分区：
文献类型：
--
作者：
BENAV, P;CROFFORD, LJ;HLA, T
炎症介质如前列腺素E（2）（PGE（2））和白细胞介素-1（IL-1）通过尚未确定的机制诱导血管生成。我们证明PGE（2）和IL-1诱导血管内皮生长因子（VEGF）的表达，VEGF是类风湿性滑膜成纤维细胞的选择性血管生成因子。PGE受体的EP（1）和EP（2）亚型的转录物在滑膜成纤维细胞中表达，蛋白激酶A通路的激活剂刺激VEGF的表达，而蛋白激酶C的下调并不影响PGE的作用，这表明EP（2）受体通过蛋白激酶A通路的信号传导是重要的。PGE（2）和白细胞介素-1 α诱导VEGF的表达可能是炎性血管生成的重要机制。
Inflammatory mediators such as prostaglandin E(2) (PGE(2)) and interleukin-l (IL-1) induce angiogenesis by yet undefined mechanisms, We demonstrate that PGE(2) and IL-1 induces the expression of vascular endothelial growth factor (VEGF), a selective angiogenic factor by rheumatoid synovial fibroblast cells, Transcripts for the EP(1) and EP(2) subtypes of PGE receptors are expressed in synovial fibroblasts, Activators of protein kinase A pathway stimulated the expression of VEGF whereas down-regulation of protein kinase C did not influence the PGE effect, suggesting that signalling from the EP(2) receptor via the protein kinase A pathway is important, The induction of VEGF expression by PGE(2) and interleukin-1 alpha may be an important mechanism in inflammatory angiogenesis.