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首页> 外文期刊>American Journal of Physiology >Fibroblast growth factor-23 increases mouse PGE2 production in vivo and in vitro.
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Fibroblast growth factor-23 increases mouse PGE2 production in vivo and in vitro.

机译：成纤维细胞生长因子-23可提高体内和体外小鼠PGE2的产量。

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摘要

Fibroblast growth factor-23 (FGF-23) has been implicated in the renal phosphate wasting in X-linked hypophosphatemia, tumor-induced osteomalacia, and autosomal dominant hypophosphatemic rickets. Recently, we demonstrated that Hyp mice have greater urinary PGE2 levels compared with C57/B6 mice and that indomethacin administration in vivo and in vitro ameliorates the phosphate transport defect in Hyp mice. To determine further whether altered prostaglandin metabolism plays a role in the renal phosphate transport defect in Hyp mice, we incubated renal proximal tubules with arachidonic acid. We find that PGE2 production was higher in Hyp mice than in C57/B6 mice. Incubation of C57/B6 mouse renal proximal tubules with FGF-23R176Q, an active mutant form of FGR23, increased tubular PGE2 production, an effect that was inhibited by 50 microM PD-98059 and 10 microM SB-203580, inhibitors of the MAP kinase pathway. C57/B6 mice injected with FGF-23R176Q had a approximately 10-fold increase in PGE2 excretion 24 h after intraperitoneal injection of FGF-23R176Q compared with vehicle-treated controls. Finally, we show that PGE2 inhibited both phosphate and volume absorption in mouse proximal convoluted tubules perfused in vitro and reduced brush-border membrane vesicle NaPi-2a protein abundance from renal cortex incubated in vitro with PGE2. In conclusion, FGF-23 increases urinary and renal tubular PGE2 production via the MAP kinase pathway and PGE2 inhibits proximal tubule phosphate transport.
机译：成纤维细胞生长因子-23（FGF-23）与X连锁性低磷血症，肿瘤引起的骨软化症和常染色体显性低磷性rick病中的肾磷酸盐消瘦有关。最近，我们证明Hyp小鼠比C57 / B6小鼠具有更高的尿PGE2水平，体内和体外给予消炎痛可改善Hyp小鼠的磷酸盐转运缺陷。为了进一步确定改变的前列腺素代谢是否在Hyp小鼠的肾脏磷酸盐转运缺陷中起作用，我们将花生四烯酸与肾脏近端小管一起孵育。我们发现，Hyp小鼠的PGE2产量高于C57 / B6小鼠。 C57 / B6小鼠肾近端小管与FGR23的活性突变体FGF-23R176Q一起孵育可增加肾小管PGE2的产生，这一作用被MAP激酶途径的抑制剂50 microM PD-98059和10 microM SB-203580抑制。与载体治疗的对照组相比，腹膜内注射FGF-23R176Q后24小时，注射FGF-23R176Q的C57 / B6小鼠的PGE2排泄增加了约10倍。最后，我们显示PGE2抑制了小鼠灌注的小鼠近曲状小管中的磷酸盐和体积吸收，并降低了与PGE2体外培养的肾皮质的刷状边界膜囊泡NaPi-2a蛋白的丰度。总之，FGF-23通过MAP激酶途径增加尿和肾小管PGE2的产生，而PGE2抑制近端小管磷酸盐的转运。

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