Hatazawa R, Tanigami M, Izumi N, Kamei K, Tanaka A, Takeuchi K
Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto 607-8414, Japan.
Inflammopharmacology. 2007 Oct;15(5):214-7. doi: 10.1007/s10787-007-1595-z.
Vascular endothelial growth factor (VEGF), a fundamental regulator of angiogenesis, plays an important role in gastric ulcer healing. In addition, prostaglandin E2 (PGE2), derived from cyclooxygenase-2, stimulates VEGF release in gastric fibroblasts. In the present study, we examined which EP receptor subtype is involved in the expression of VEGF in primary rat gastric fibroblasts. PGE2 stimulated VEGF protein expression in the fibroblasts in a time- and dose-dependent manner. The up-regulation by PGE2 of VEGF expression was completely inhibited by a subtype selective EP4 receptor antagonist (AE3-208). Furthermore, the selective EP4 receptor agonist, AE1-329, promoted VEGF expression in the fibroblasts, and this effect was also totally antagonized by AE3-208. These results suggest that PGE2 stimulates VEGF expression in gastric fibroblasts through the activation of EP4 receptors, and this effect may be involved in the healing promoting action of PGE2 on gastric ulcers.
血管内皮生长因子(VEGF)是血管生成的重要调节因子,在胃溃疡愈合中起重要作用。此外,源自环氧化酶-2的前列腺素E2(PGE2)可刺激胃成纤维细胞释放VEGF。在本研究中,我们检测了哪种EP受体亚型参与原代大鼠胃成纤维细胞中VEGF的表达。PGE2以时间和剂量依赖性方式刺激成纤维细胞中VEGF蛋白表达。VEGF表达的PGE2上调被亚型选择性EP4受体拮抗剂(AE3-208)完全抑制。此外,选择性EP4受体激动剂AE1-329促进成纤维细胞中VEGF表达,且该作用也被AE3-208完全拮抗。这些结果表明,PGE2通过激活EP4受体刺激胃成纤维细胞中VEGF表达,且该作用可能参与PGE2对胃溃疡的愈合促进作用。