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首页> 美国卫生研究院文献>American Journal of Respiratory Cell and Molecular Biology >Prostaglandin E2 Inhibits Human Lung Fibroblast Chemotaxis through Disparate Actions on Different E-Prostanoid Receptors
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Prostaglandin E2 Inhibits Human Lung Fibroblast Chemotaxis through Disparate Actions on Different E-Prostanoid Receptors

机译：前列腺素E2通过对不同的E-前列腺素受体的不同作用抑制人肺成纤维细胞趋化性。

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摘要

The migration of fibroblasts is believed to play a key role in both normal wound repair and abnormal tissue remodeling. Prostaglandin E (PGE)2, a mediator that can inhibit many fibroblast functions including chemotaxis, was reported to be mediated by the E-prostanoid (EP) receptor EP2. PGE2, however, can act on four receptors. This study was designed to determine if EP receptors, in addition to EP2, can modulate fibroblast chemotaxis. Using human fetal lung fibroblasts, the expression of all four EP receptors was demonstrated by Western blotting. EP2-selective and EP4-selective agonists inhibited both chemotaxis toward fibronectin in the blindwell assay and migration in a wound-closure assay. In contrast, EP1-selective and EP3-selective agonists stimulated cell migration in both assay systems. These results were confirmed using EP-selective antagonists. The role of both EP2 and EP4 receptors in mediating the PGE2 inhibition of chemotaxis was also confirmed by small interfering RNA suppression. Furthermore, the role of EP receptors was confirmed by blocking the expected signaling pathways. Taken together, these results demonstrate that PGE2 can act on multiple EP receptors in human lung fibroblasts, to exert disparate effects. Alterations in EP receptor expression may have the potential to alter PGE2 action. Targeting specific EP receptors may offer therapeutic opportunities in conditions characterized by abnormal tissue repair and remodeling.
机译：据信成纤维细胞的迁移在正常伤口修复和异常组织重塑中都起关键作用。前列腺素E（PGE）2是一种可以抑制许多成纤维细胞功能（包括趋化性）的介体，据报道是由E-前列腺素（EP）受体EP2介导的。但是，PGE2可以作用于四个受体。这项研究旨在确定除EP2外，EP受体是否可以调节成纤维细胞的趋化性。使用人胎肺成纤维细胞，通过蛋白质印迹法证实了所有四种EP受体的表达。 EP2选择性和EP4选择性激动剂在盲孔试验中抑制了对纤连蛋白的趋化作用，而在伤口闭合试验中则抑制了迁移。相反，EP1选择性和EP3选择性激动剂在两种测定系统中均能刺激细胞迁移。使用EP选择性拮抗剂证实了这些结果。小干扰RNA抑制也证实了EP2和EP4受体在介导PGE2抑制趋化性中的作用。此外，通过阻断预期的信号通路，证实了EP受体的作用。综上所述，这些结果表明PGE2可以作用于人肺成纤维细胞中的多种EP受体，发挥不同的作用。 EP受体表达的改变可能具有改变PGE2作用的潜力。在异常组织修复和重塑为特征的情况下，靶向特定的EP受体可能提供治疗机会。

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