Role of the putative PKC phosphorylation sites of the type IIc sodium-dependent phosphate transporter in parathyroid hormone regulation

Fujii, Tomoyuki; Segawa, Hiroko; Hanazaki, Ai; Nishiguchi, Shiori; Minoshima, Sakura; Ohi, Akiko; Tominaga, Rieko; Sasaki, Shiro; Tanifuji, Kazuya; Koike, Megumi; Arima, Yuki; Shiozaki, Yuji; Kaneko, Ichiro; Ito, Mikiko; Tatsumi, Sawako; Miyamoto, Ken‐ichi

doi:10.1007/s10157-019-01725-6

Cited by 9 publications

(8 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PTH also increases renal PO 4 excretion at proximal tubule of the kidney by reducing apical membrane NaPi II a and II c [14,33,34]. Moreover, PTH increases FGF-23 gene expression [35].…”

Section: Discussionmentioning

confidence: 99%

“…FGF-23 decreases serum PO 4 by inhibiting renal PO 4 reabsorption through FGF-23-Klotho (coreceptor) signaling on NaPi II a and II c at proximal tubule of the kidney. FGF-23 also suppresses 1,25-dihydroxyvitamin D (1,25(OH)2 D) production by decreasing 1αhydroxylase expression [12][13][14]. PTH promotes PO 4 excretion by suppressing NaPi-II in the kidney [15].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2020

View full text Add to dashboard Cite

Background: phosphate homeostasis is mediated through complex counter regulatory feedback balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium-phosphate cotransporters II a and II c. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods: In this case-control study, 19 patients with hypoparathyroidism and their age-and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results: The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group (P < 0.001 and P < 0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P < 0.001 and P < 0.001, respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P < 0.001, r = 0.79). Conclusions: Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

show abstract

“…PTH also increases renal PO 4 excretion at proximal tubule of the kidney by reducing apical membrane NaPi II a and II c [14,33,34]. Moreover, PTH increases FGF-23 gene expression [35].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2020

View full text Add to dashboard Cite

show abstract

“…For exogenous FGF23 expression, TransIT-EE Hydrodynamic Delivery Solution was used as the TransIT in vivo gene delivery system (Takara, Osaka, Japan) as described previously 26,27 . For PTH injection, mice were administered bovine PTH (amino acid 1-34; Sigma) at a dose of 7.5 µg/100 g body weight, as described previously 50,51 .…”

Section: Effect Of Fgf23 and Pth On The Regulation Of Napi Transporter Degradationmentioning

confidence: 99%

Phosphate Transporter Regulator That Prevents Abnormal Hyperphosphatemia.

Sasaki

Shiozaki

Hanazaki

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. A high Pi load induces the phosphaturic hormones parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), enhances urinary Pi excretion and prevents the onset of hyperphosphatemia. How FGF23 is induced from the bones by a high Pi load and the setpoint of the plasma Pi concentration, however, are unclear. Here, we investigated the role of transporter-associated protein (TRAP), found in gene co-expression networks in NaPi2a and NaPi2c function. TRAP is localized in the renal proximal tubules and interacts with NaPi2a. In TRAP-knockout (KO) mice, the serum FGF23 concentration was markedly increased but increased Pi excretion and hypophosphatemia were not observed. In addition, TRAP-KO mice exhibit reduced NaPi2a responsiveness to FGF23 and PTH administration. Furthermore, a dietary Pi load causes marked hyperphosphatemia and abnormal NaPi2a regulation in TRAP-KO mice. Thus, TRAP is thought to be associated with FGF23 induction in bones and the regulation of NaPi2a to prevent an increase in the plasma Pi concentration due to a high Pi load and kidney injury.

show abstract

“…PO 4 serum concentration is kept within the normal range by a complex regulation between intestinal absorption, renal filtration-reabsorption, and bone resorption of PO 4 mediated by regulatory hormones [9][10][11]. The most important hormones that regulate tubular PO 4 1α-hydroxylase expression [12][13][14]. PTH promotes PO 4 excretion by suppressing NaPi-II in the kidney [15].…”

Section: Introductionmentioning

confidence: 99%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

View full text Add to dashboard Cite

Background phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters IIa and IIc. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal control population(P <0.001, r = 0.79). Conclusions Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

show abstract

Role of the putative PKC phosphorylation sites of the type IIc sodium-dependent phosphate transporter in parathyroid hormone regulation

Cited by 9 publications

References 38 publications

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Phosphate Transporter Regulator That Prevents Abnormal Hyperphosphatemia.

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Contact Info

Product

Resources

About