scholarly journals Genetic evidence of the regulatory role of parathyroid hormone-related protein in articular chondrocyte maintenance in an experimental mouse model

2011 ◽  
Vol 63 (11) ◽  
pp. 3333-3343 ◽  
Author(s):  
Carolyn Macica ◽  
Guoying Liang ◽  
Ali Nasiri ◽  
Arthur E. Broadus
Keyword(s):  
Parathyroid Hormone ◽  
Mouse Model ◽  
Genetic Evidence ◽  
Regulatory Role ◽  
Related Protein ◽  
Articular Chondrocyte ◽  
Parathyroid Hormone Related Protein ◽  
Experimental Mouse Model ◽  
Experimental Mouse

scholarly journals Parathyroid hormone-related protein as predictor of urolithiasis disease development

2020 ◽  
pp. 41-46
Author(s):  
A. A. Budanov ◽  
V. L. Medvedev ◽  
A. N. Kurzanov ◽  
A. A. Basov ◽  
G. A. Palaguta ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Surgical Treatment ◽  
Blood Parameters ◽  
Scientific Research Institute ◽  
Healthy People ◽  
Disease Development ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Recurrent Nephrolithiasis

Background. The present article studies a possible role of parathyroid hormone-related protein (PTHrP) in urolithiasis pathogenesis.Aim. To consider PTHrP level as a predictor of the urolithiasis development.Material and methods. We presented an analysis of treatment in 79 patients with primary and recurrent nephrolithiasis that had underwent surgical treatment in the Uronephrological Center of Scientific Research Institute – Ochapovsky Regional Clinical Hospital #1, Krasnodar from 2017 to 2019. All observed patients were divided in two groups: patients with primary and recurrent nephrolithiasis. A group of 10 relatively healthy people was included in the study as well. All patients and conditionally healthy people had a test for blood parameters; in particular, the level of parathyroid hormone-related protein was assessed in order to compare the indicators in all three groups.Conclusions. The PTHrP level was showed to be statistically significantly different in patients with urolithiasis from the group with relatively healthy people. Groups with primary and recurrent nephrolithiasis show not difference in the level of PTHrP. Further studies are necessary to consider this protein as one of the predictors of urolithiasis and study its role in the pathogenesis of nephrolithiasis.

The role of fetal parathyroid hormone-related protein in transplacental calcium transport

1996 ◽  
Vol 17 (2) ◽  
pp. 159-164 ◽  
Author(s):  
J Tucci ◽  
V Hammond ◽  
P V Senior ◽  
A Gibson ◽  
F Beck
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Pump ◽  
Calcium Deposition ◽  
Related Protein ◽  
Compensatory Mechanisms ◽  
Total Body Calcium ◽  
Parathyroid Hormone Related Protein ◽  
Ionised Calcium ◽  
Total Body

ABSTRACT During pregnancy, a placental calcium pump maintains the fetus in a hypercalcaemic state relative to the mother, a condition which has been thought to facilitate normal development of the fetal skeleton. Based on experiments performed in the sheep, parathyroid hormone-related protein (PTHrP) has been implicated as the hormone responsible for maintaining the placental calcium pump. In the present study on mice in which the PTHrP gene has been ablated by homologous recombination, we have measured both fetal and maternal circulating total and ionised calcium levels, as well as fetal total body calcium, in order to determine whether absence of PTHrP during fetal development has an effect on fetal calcium levels. Our results show that, in fetuses lacking PTHrP, circulating ionised calcium levels are significantly lower than those of heterozygote and wild-type littermates, but circulating total calcium levels show no difference. Total body calcium levels of null mutants are significantly higher than those of normal littermates. The role of PTHrP in maintaining the integrity of the transplacental calcium pump in the rodent thus remains unclear. It may be that the lower levels of fetal blood ionised calcium in mutant animals are due to disruption of the placental pump, but, if this is the case, compensatory mechanisms have operated to allow the excessive calcium deposition seen in the skeletons of these animals. Alternatively, the increased avidity of the bones for calcium may in itself have produced a lower equilibrium level of available ionised calcium.

Role of the fetal parathyroid glands and parathyroid hormone-related protein in the regulation of placental transport of calcium, magnesium and inorganic phosphate

1991 ◽  
Vol 3 (4) ◽  
pp. 447 ◽  
Author(s):  
RJ MacIsaac ◽  
JA Heath ◽  
CP Rodda ◽  
JM Moseley ◽  
AD Care ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Autologous Blood ◽  
Placental Tissue ◽  
Parathyroid Glands ◽  
Related Protein ◽  
Tissue Extracts ◽  
Parathyroid Hormone Related Protein ◽  
Placental Transport ◽  
Calcium Magnesium

The plasma Ca concentration of the fetus is maintained higher than maternal levels by active placental transport. Ca, Mg and PO4 accumulation by the fetus is mainly associated with skeletal growth. The fetal parathyroid glands are essential for maintenance of elevated plasma Ca, which is necessary for the stimulation of fetal osteoblasts and mineralization of cartilage and osteoid. Fetal thyroparathyroidectomy (TxPTx) results in a decreased activity of the placental Ca pump. The presence of a parathyroid hormone-related protein (PTHrP) has been demonstrated in fetal parathyroid glands and placental tissue. Extracts of fetal parathyroid glands and purified PTHrP, as well as recombinant PTHrP (1-84, 1-108 and 1-141), stimulate Ca and Mg but not PO4 transport across the placenta of TxPTx-ized fetuses perfused with autologous blood in the absence of the fetus. Parathyroid hormone (PTH) and the N-terminal region of PTHrP do not stimulate placental Ca and Mg transport. It is concluded that a mid-molecule region of this novel hormone may be required to stimulate placental Ca transfer and contribute to the regulation of fetal Ca homeostasis.

scholarly journals Parathyroid Hormone-Related Protein (PTHrP) Accelerates Soluble RANKL Signals for Downregulation of Osteogenesis of Bone Mesenchymal Stem Cells

2019 ◽  
Vol 8 (6) ◽  
pp. 836 ◽  
Author(s):  
Jeevithan Elango ◽  
Saeed Ur Rahman ◽  
Yves Henrotin ◽  
José Eduardo Maté Sánchez de Val ◽  
Bin Bao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Parathyroid Hormone ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Related Protein ◽  
Bone Mesenchymal Stem Cells ◽  
Parathyroid Hormone Related Protein ◽  
Receptor Activator

A recent study reported the expression of receptor activator of nuclear factor-κB (RANK) in mesenchymal stem cells (MSCs) surface that negatively regulates osteogenesis of MSCs. Empirical evidence from the previous study confirmed the role of parathyroid hormone-related protein (PTHrP) in osteoblastogenesis. However, it is necessary to understand the paracrine role of PTHrP and RANKL for osteogenesis in order to explore the hidden secrets in bone biology. Considering the above concept, paracrine cues of soluble-receptor activator of nuclear factor-κB ligand (sRANKL) and PTHrP in osteogenic differentiation of MSCs were investigated. Our results confirmed that sRANKL increased the expression of surface-RANK in MSCs at the earlier stage of osteogenesis, which was downregulated later in differentiated MSCs. In contrast, RANKL expression was low at the earlier stage of MSCs proliferation and high at the differentiation stage of MSCs, which may play a fundamental role in osteoclast formation. sRANKL downregulated osteogenesis of MSCs by decreasing progressive ankylosis (ANK) protein expression while PTHrP upregulated the osteogenic exploitive effect of sRANKL. Interestingly, when they were co-cultured with MSCs, T-lymphocytes expressed high membrane-RANKL levels that contribute to osteogenesis inhibition during MSC differentiation. Thus, our results disclose that sRANKL treatment downregulates osteogenesis of MSCs by increasing RANK expression at the earlier stage of differentiation and by inhibiting ANK. Further, we demonstrated that PTHrP accelerated the downregulating osteogenic effect of sRANKL.

Role of the N- and C-terminal Fragments of Parathyroid-Hormone-Related Protein as Putative Therapies to Improve Bone Regeneration Under High Glucocorticoid Treatment

2010 ◽  
Vol 16 (4) ◽  
pp. 1157-1168 ◽  
Author(s):  
Luís Fernándes de Castro ◽  
Daniel Lozano ◽  
Sonia Dapía ◽  
Sergio Portal-Núñez ◽  
José R. Caeiro ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Regeneration ◽  
Related Protein ◽  
Glucocorticoid Treatment ◽  
Parathyroid Hormone Related Protein
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