A basic study of de novo function of PTH in mineral metabolism disorders

PTH增加了大鼠颅骨源性成骨细胞培养中Fgf23启动子的活性，但Fgf23mRNA的表达和产生水平没有显著变化。另一方面，PTH与二羟基维生素D3（1,25 d）联合使用时，可降低1,25 d诱导的Fgf23mRNA的表达和产生。造成这种影响的原因之一是PTH抑制了维生素D受体和III型钠依赖性磷酸盐转运体（Pit1）的表达。PTH通过PKA途径促进MKP1磷酸化，从而减弱FGF23信号。

PTH increased the promoter activity of Fgf23 in rat calvaria-derived osteoblast cell cultures, however, there was no significant change in the levels of Fgf23mRNA expression and production. In combination with dihydroxyvitamin D3(1,25D), on the other hand, PTH decreased 1,25D-induced Fgf23mRNA expression and production. One of the reasons for this effect is that the expression of vitamin D receptor and type III sodium-dependent phosphate transporter (Pit1) was suppressed by PTH. Further, PTH promoted MKP1 phosphorylation via PKA pathway, and thereby attenuated the signal FGF23 signaling.