Endocrinology of Bone and Growth Disorders

Farquharson, Colin; Stephen, Louise A.; Wong, Sze Choong

doi:10.1016/b978-0-12-820472-6.00086-4

Cited by 1 publication

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“…This function is essential to prevent disturbance to a range of cellular functions and is mediated by interactions with the PTH1 receptor in key target tissues such as bone, kidney and intestine. 1,2 PTH also maintains phosphate homoeostasis by several mechanisms including the promotion of osteocyte synthesis of fibroblast growth factor 23 (FGF23) which, in conjunction with cofactor klotho and via the renal FGF receptor, promotes phosphaturia by downregulating sodium-phosphate cotransporter (Npt2a and Npt2c) expression. 3 In addition to increasing osteoclast bone resorption to mobilise Ca2+, PTH also has profound effects on the cells of the osteoblast lineage and is now regarded as an important hormone regulating bone remodelling.…”

Section: Take Down Policymentioning

confidence: 99%

“…Parathyroid hormone (PTH) is synthesised and secreted by the chief cells of the parathyroid glands to maintain serum calcium (Ca2+) concentrations within a very narrow range. This function is essential to prevent disturbance to a range of cellular functions and is mediated by interactions with the PTH1 receptor in key target tissues such as bone, kidney and intestine 1,2 . PTH also maintains phosphate homoeostasis by several mechanisms including the promotion of osteocyte synthesis of ﬁbroblast growth factor 23 (FGF23) which, in conjunction with cofactor klotho and via the renal FGF receptor, promotes phosphaturia by downregulating sodium–phosphate cotransporter (Npt2a and Npt2c) expression 3 …”

Section: Introductionmentioning

confidence: 99%

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Increased PHOSPHO1 and alkaline phosphatase expression during the anabolic bone response to intermittent parathyroid hormone delivery

Houston

Stephen

Jayash

et al. 2022

Cell Biochemistry & Function

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The administration of intermittent parathyroid hormone (iPTH) is anabolic to the skeleton. Recent studies with cultured osteoblasts have revealed that the expression of PHOSPHO1, a bone-specific phosphatase essential for the initiation of mineralisation, is regulated by PTH. Therefore, this study sought to determine whether the bone anabolic response to iPTH involves modulation of expression of Phospho1 and of other enzymes critical for bone matrix mineralisation. To mimic iPTH treatment, primary murine osteoblasts were challenged with 50 nM PTH for 6 h in every 48 h period for 8 days (4 cycles), 14 days (7 cycles) and 20 days (10 cycles) in total. The expression of both Phospho1 and Smpd3 was almost completely inhibited after 4 cycles, whereas 10 cycles were required to stimulate a similar response in Alpl expression. To explore the in vivo role of PHOSPHO1 in PTH-mediated osteogenesis, the effects of 14-and 28-day iPTH (80 μg/kg/day) administration was assessed in male wild-type (WT) and Phospho1 −/− mice. The expression of Phospho1, Alpl, Smpd3, Enpp1, Runx2 and Trps1 expression was enhanced in the femora of WT mice following iPTH administration but remained unchanged in the femora of Phospho1 −/− mice. After 28 days of iPTH administration, the anabolic response in the femora of WT was greater than that noted in Phospho1 −/− mice. Specifically, cortical and trabecular bone volume/total volume, as well as cortical thickness, were increased in femora of iPTH-treated WT but not in iPTH-treated Phospho1 −/− mice. Trabecular bone osteoblast number was also increased in iPTH-treated WT mice but not in iPTH-treated Phospho1 −/− mice. The increased levels of Phospho1, Alpl, Enpp1 and Smpd3 in WT mice in response to iPTH administration is consistent with their contribution to the potent anabolic properties of iPTH in bone. Furthermore, as the anabolic response to iPTH was attenuated in

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Section: Take Down Policymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%