Готові списки джерел за темами / Parathyroid Hormone Receptor (PTH1R)

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Добірка наукової літератури з теми "Parathyroid Hormone Receptor (PTH1R)"

Автор: Grafiati
Опубліковано: 10 березня 2023

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Статті в журналах з теми "Parathyroid Hormone Receptor (PTH1R)"

1

Sneddon, W. Bruce, Yanmei Yang, Jianming Ba, Lisa M. Harinstein, and Peter A. Friedman. "Extracellular signal-regulated kinase activation by parathyroid hormone in distal tubule cells." American Journal of Physiology-Renal Physiology 292, no. 3 (March 2007): F1028—F1034. http://dx.doi.org/10.1152/ajprenal.00288.2006.

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Анотація:
The PTH receptor (PTH1R) activates multiple signaling pathways, including extracellular signal-regulated kinases 1 and 2 (ERK1/2). The role of epidermal growth factor receptor (EGFR) transactivation in ERK1/2 activation by PTH in distal kidney cells, a primary site of PTH action, was characterized. ERK1/2 phosphorylation was stimulated by PTH and blocked by the EGFR inhibitor, AG1478. Upon PTH stimulation, metalloprotease cleavage of membrane-bound heparin-binding fragment (HB-EGF) induced EGFR transactivation of ERK. Conditioned media from PTH-treated distal kidney cells activated ERK in HEK-293 cells. AG1478 added to HEK-293 cells ablated transactivation by conditioned media. HB-EGF directly activated ERK1/2 in HEK-293 cells. Pretreatment of distal kidney cells with the metalloprotease inhibitor GM-6001 abolished transactivation of ERK1/2 by PTH. The role of the PTH1R COOH terminus in PTX-sensitive ERK1/2 activation was characterized in HEK-293 cells transfected with wild-type PTH1R, with a PTH1R mutated at its COOH terminus, or with PTH1R truncated at position 480. PTH stimulated ERK by wild-type, mutated and truncated PTH1Rs 21-, 27- and 57-fold, respectively. Thus, the PTH1R COOH terminus exerts an inhibitory effect on ERK activation. EBP50, a scaffolding protein that binds to the PDZ recognition domain of the PTH1R, impaired PTH but not isoproterenol or calcitonin-induced ERK activation. Pertussis toxin inhibited PTH-stimulated ERK1/2 by mutated and truncated PTH1Rs and abolished ERK1/2 activation by wild-type PTH1R. We conclude that ERK phosphorylation in distal kidney cells by PTH requires PTH1R activation of Gi, which leads to stimulation of metalloprotease-mediated cleavage of HB-EGF and transactivation of the EGFR and is regulated by EBP50.
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2

Bhattacharya, Poulomi, Yi Lin Yan, John Postlethwait, and David A. Rubin. "Evolution of the vertebrate pth2 (tip39) gene family and the regulation of PTH type 2 receptor (pth2r) and its endogenous ligand pth2 by hedgehog signaling in zebrafish development." Journal of Endocrinology 211, no. 2 (August 31, 2011): 187–200. http://dx.doi.org/10.1530/joe-10-0439.

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Анотація:
In mammals, parathyroid hormone (PTH), secreted by parathyroid glands, increases calcium levels in the blood from reservoirs in bone. While mammals have two PTH receptor genes, PTH1R and PTH2R, zebrafish has three receptors, pth1r, pth2r, and pth3r. PTH can activate all three zebrafish Pthrs while PTH2 (alias tuberoinfundibular peptide 39, TIP39) preferentially activates zebrafish and mammalian PTH2Rs. We know little about the roles of the PTH2/PTH2R system in the development of any animal. To determine the roles of PTH2 and PTH2R during vertebrate development, we evaluated their expression patterns in developing zebrafish, observed their phylogenetic and conserved synteny relationships with humans, and described the genomic organization of pth2, pth2r, and pth2r splice variants. Expression studies showed that pth2 is expressed in cells adjacent to the ventral part of the posterior tuberculum in the diencephalon, whereas pth2r is robustly expressed throughout the central nervous system. Otic vesicles express both pth2 and pth2r, but heart expresses only pth2. Analysis of mutants showed that hedgehog (Hh) signaling regulates the expression of pth2 transcripts more than that of nearby gnrh2-expressing cells. Genomic analysis showed that a lizard, chicken, and zebra finch lack a PTH2 gene, which is associated with an inversion breakpoint. Likewise, chickens lack PTH2R, while humans lack PTH3R, a case of reciprocally missing ohnologs (paralogs derived from a genome duplication). The considerable evolutionary conservation in genomic structure, synteny relationships, and expression of zebrafish pth2 and pth2r provides a foundation for exploring the endocrine roles of this system in developing vertebrate embryos.
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3

Atchison, Douglas K., Pamela Harding, M. Cecilia Ortiz-Capisano, Edward L. Peterson, and William H. Beierwaltes. "Parathyroid hormone stimulates juxtaglomerular cell cAMP accumulation without stimulating renin release." American Journal of Physiology-Renal Physiology 303, no. 8 (October 15, 2012): F1157—F1165. http://dx.doi.org/10.1152/ajprenal.00269.2012.

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Анотація:
Parathyroid hormone (PTH) is positively coupled to the generation of cAMP via its actions on the PTH1R and PTH2R receptors. Renin secretion from juxtaglomerular (JG) cells is stimulated by elevated intracellular cAMP, and every stimulus that increases renin secretion is thought to do so via increasing cAMP. Thus we hypothesized that PTH increases renin release from primary cultures of mouse JG cells by elevating intracellular cAMP via the PTH1R receptor. We found PTH1R, but not PTH2R, mRNA expressed in JG cells. While PTH increased JG cell cAMP content from (log10 means ± SE) 3.27 ± 0.06 to 3.92 ± 0.12 fmol/mg protein ( P < 0.001), it did not affect renin release. The PTH1R-specific agonist, parathyroid hormone-related protein (PTHrP), also increased JG cell cAMP from 3.13 ± 0.09 to 3.93 ± 0.09 fmol/mg protein ( P < 0.001), again without effect on renin release. PTH2R receptor agonists had no effect on cAMP or renin release. PTHrP increased cAMP in the presence of both low and high extracellular calcium from 3.31 ± 0.17 to 3.83 ± 0.20 fmol/mg protein ( P < 0.01) and from 3.29 ± 0.18 to 3.63 ± 0.22 fmol/mg protein ( P < 0.05), respectively, with no effect on renin release. PTHrP increased JG cell cAMP in the presence of adenylyl cyclase-V inhibition from 2.85 ± 0.17 to 3.44 ± 0.14 fmol/mg protein ( P < 0.001) without affecting renin release. As a positive control, forskolin increased JG cell cAMP from 3.39 ± 0.13 to 4.48 ± 0.07 fmol/mg protein ( P < 0.01) and renin release from 2.96 ± 0.10 to 3.29 ± 0.08 ng ANG I·mg prot−1·h−1 ( P < 0.01). Thus PTH increases JG cell cAMP via non-calcium-sensitive adenylate cyclases without affecting renin release. These data suggest compartmentalization of cAMP signaling in JG cells.
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4

Gensure, Robert C., Bhaskar Ponugoti, Yasemin Gunes, Madhusudhan R. Papasani, Beate Lanske, Murat Bastepe, David A. Rubin, and Harald Jüppner. "Identification and Characterization of Two Parathyroid Hormone-Like Molecules in Zebrafish." Endocrinology 145, no. 4 (April 1, 2004): 1634–39. http://dx.doi.org/10.1210/en.2003-0964.

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Анотація:
Abstract Zebrafish (Danio rerio) have receptors homologous to the human PTH (hPTH)/PTHrP receptor (PTH1R) and PTH-2 receptor (PTH2R) and an additional receptor (PTH3R) with high homology to the PTH1R. To find natural ligands for zPTH1R and zPTH3R, we searched the zebrafish genomic database and discovered two distinct regions that, when translated (zPTH1 and zPTH2), showed high homology to hPTH. Isolation of cDNAs and determination of the intron/exon boundaries revealed genomic structures which were similar to known PTHs. Peptides consisting of the first 34 amino acids after the pre- and prosequences of the zebrafish PTHs (zPTHs) were synthesized and were shown to be fully active at the hPTH1R. zPTH2(1–34) was, however, approximately 30-fold less potent at the zPTH1R than hPTH(1–34), hPTHrP(1–36), and zPTH1(1–34). When tested with zPTH3R, zPTH1(1–34) and hPTHrP(1–36) showed similar potencies, whereas the potency of zPTH2(1–34) was moderately (3-fold) reduced. To determine whether other fishes have multiple PTHs, we searched the genomic database of the Japanese pufferfish (Takifugu rubripes) and identified zPTH1 and zPTH2 homologs. Phylogenetic analysis showed that PTHs from zebrafish and pufferfish are more closely related to each other than to known mammalian PTH homologs or to PTHrP and tuberoinfundibular peptide of 39 residues. This is consistent with evolution of two teleost PTH-like peptides occurring after the evolutionary divergence between fishes and mammals. Overall, the PTH system appears more complex in fishes than in mammals, providing evidence of continued evolution in nontetrapod species. The availability of multiple forms of fish PTH and their receptors provide additional tools for PTH ligand/receptor structure-function studies.
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5

Mannstadt, Michael, Harald Jüppner, and Thomas J. Gardella. "Receptors for PTH and PTHrP: their biological importance and functional properties." American Journal of Physiology-Renal Physiology 277, no. 5 (November 1, 1999): F665—F675. http://dx.doi.org/10.1152/ajprenal.1999.277.5.f665.

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Анотація:
The type 1 receptor (PTH1R) for parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) is a G protein-coupled receptor that is highly expressed in bone and kidney and mediates in these tissues the PTH-dependent regulation of mineral ion homeostasis. The PTH1R also mediates the paracrine actions of PTHrP, which play a particularly vital role in the process of endochondral bone formation. These important functions, the likely involvement of the PTH1R in certain genetic diseases affecting skeletal development and calcium homeostasis, and the potential utility of PTH in treating osteoporosis have been the driving force behind intense investigations of both the receptor and its peptide ligands. Recent lines of work have led to the identification of constitutively active PTH1Rs in patients with Jansen's metaphyseal chondrodysplasia, the demonstration of inverse agonism by certain ligand analogs, and the discovery of the PTH-2 receptor subtype that responds to PTH but not PTHrP. As reviewed herein, a detailed exploration of the receptor-ligand interaction process is currently being pursued through the use of site-directed mutagenesis and photoaffinity cross-linking methods; ultimately, such work could enable the development of novel PTH receptor ligands that have therapeutic value in treating diseases such as osteoporosis and certain forms of hypercalcemia.
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6

Miedlich, Susanne U., and Abdul B. Abou-Samra. "Eliminating phosphorylation sites of the parathyroid hormone receptor type 1 differentially affects stimulation of phospholipase C and receptor internalization." American Journal of Physiology-Endocrinology and Metabolism 295, no. 3 (September 2008): E665—E671. http://dx.doi.org/10.1152/ajpendo.00036.2008.

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Анотація:
The parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor (PTH1R) belongs to family B of seven-transmembrane-spanning receptors and is activated by PTH and PTHrP. Upon PTH stimulation, the rat PTH1R becomes phosphorylated at seven serine residues. Elimination of all PTH1R phosphorylation sites results in prolonged cAMP accumulation and impaired internalization in stably transfected LLC-PK1 cells. The present study explores the role of individual PTH1R phosphorylation sites in PTH1R signaling through phospholipase C, agonist-dependent receptor internalization, and regulation by G protein-coupled receptor kinases. By means of transiently transfected COS-7 cells, we demonstrate that the phosphorylation-deficient (pd) PTH1R confers dramatically enhanced coupling to Gq/11 proteins upon PTH stimulation predominantly caused by elimination of Ser491/492/493, Ser501, or Ser504. Reportedly, impaired internalization of the pd PTH1R, however, is not dependent on a specific phosphorylation site. In addition, we show that G protein-coupled receptor kinase 2 interferes with pd PTH1R signaling to Gq/11 proteins at least partially by direct binding to Gq/11 proteins.
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7

Sneddon, W. Bruce, та Peter A. Friedman. "β-Arrestin-Dependent Parathyroid Hormone-Stimulated Extracellular Signal-Regulated Kinase Activation and Parathyroid Hormone Type 1 Receptor Internalization". Endocrinology 148, № 8 (1 серпня 2007): 4073–79. http://dx.doi.org/10.1210/en.2007-0343.

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Анотація:
PTH regulates renal calcium homeostasis by actions on the distal nephron. PTH-induced calcium transport in mouse distal convoluted tubule (DCT) cells requires activation of ERK1/2. ERK activation by β-adrenergic receptors occurs in a biphasic manner and involves receptor internalization. An early rapid phase is β-arrestin (βAr) independent, whereas prolonged activation is βAr dependent. We characterized PTH-stimulated ERK activation and the involvement of receptor internalization and βAr dependence. In DCT cells, PTH transiently activated ERK maximally at 5 min and then returned to baseline. βAr dependence of PTH receptor (PTH1R)-mediated ERK stimulation was assessed using mouse embryonic fibroblasts (MEFs) from βAr1- and -2-null mice. In wild-type MEFs, PTH(1–34)-stimulated ERK activation peaked after 5 min, was 50% maximal after 15 min, and then recovered to 80% of maximal stimulation by 30 min. In MEFs null for βAr1 and -2, PTH-stimulated ERK activation peaked by 5 min and returned to baseline. The effect was identical in βAr2-null MEFs. In βAr1-null MEFs, ERK exhibited delayed activation and remained elevated. PTH-stimulated ERK activation and receptor endocytosis were not inhibited by the clathrin-binding domain of βAr1 [Ar(319–418)]. Coexpression of the sodium proton exchanger regulatory factor 1 (NHERF1) with Ar(319–418) blocked PTH1R internalization. We conclude that PTH-stimulated ERK activation in DCT cells proceeds with a rapid but transient phase that may involve βAr1. Furthermore, the βAr-dependent late phase of ERK activation by PTH requires the participation of βAr2 and PTH1R internalization.
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8

Izquierdo-Lahuerta, Adriana. "The Parathyroid Hormone-Related Protein/Parathyroid Hormone 1 Receptor Axis in Adipose Tissue." Biomolecules 11, no. 11 (October 22, 2021): 1570. http://dx.doi.org/10.3390/biom11111570.

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Анотація:
Adipose tissue is an organ that shows great plasticity and is able to adapt to the conditions to which the body is subdued. It participates in the regulation of energetic homeostasis and has endocrine functions. Recent studies have shown how the parathyroid hormone-related protein (PTHrP)/Parathyroid Hormone Receptor 1 (PTH1R) axis participates in the regulation of adipogenesis, opposing the action of Peroxisome proliferator-activated receptor gamma (PPARγ). In addition to this, PTHrP is overexpressed in adipose tissue in situations of wear and tear of the body, favoring browning and lipolysis in this tissue. It is also overexpressed in adipose tissue in stressful situations but in the opposite direction, in obesity, metabolic syndrome, type 2 diabetes mellitus (T2DM) and gestational diabetes mellitus (GDM). In conclusion, the PTHrP/PTH1R axis has a main role in adipose tissue, participating in its differentiation and remodeling. PTHrP might be used in obesity treatment and its complications for its ability to reprogram adipogenesis and adipose tissue expansion, WAT browning and for the improvement of the insulin sensitivity. In addition, PTHrP could even be used as a marker of placental status and maternal adaptations to prevent future metabolic problems in mothers and children, as well as in the treatment of bone-related diseases such as osteoporosis.
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9

Danz, Jan. "Zahneruption und Zahnbewegung bei kongenitaler Retention mit Mutation des PTH1-Rezeptor-Gens." Informationen aus Orthodontie & Kieferorthopädie 50, no. 03 (September 2018): 169–75. http://dx.doi.org/10.1055/a-0648-8013.

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ZusammenfassungDie primäre kongenitale Retention von Zähnen des Typs heterozygote Mutation von Parathyroid hormone receptor type 1 (PTH1R) mit autosomal dominanter Vererbung ist eine Regulationsstörung des Knochenumbaus, welche die Zahneruption und die Zahnbewegungen stark behindert oder verhindert. Bei beginnender Zahneruption und bei Zahnbewegung wird PTHrP (Parathyroid hormone-related protein) ausgeschüttet, welches durch Osteozyten den Knochenumbau Richtung Knochenresorption entkoppelt. Bei PTH1R-Mutation mit Funktionsverlust dieses Rezeptors fehlt einerseits die Verringerung der Osteoprotegerin (OPG)- und der Sclerostin-Ausschüttung durch Osteozyten und andererseits die erhöhte Expression und Ausschüttung von Soluble receptor activator of nuclear factor κB (sRANKL) durch Osteozyten und Osteoblasten, was zu einer ausbleibenden Osteoklastenaktivierung führt. Ohne Knochenresorption durch Osteoklasten sind sowohl die Zahneruption als auch die Zahnbewegung gestört. Durch das als kompetitiver Antagonist des wnt-Rezeptor-Komplexes (kanonischer-wnt-Signalweg) und der BMP-I/BMP-II-Rezeptoren wirkende Sclerostin modulieren Osteozyten auch die Osteoblastenaktivität. Bei Verdacht auf kongenitale Retention ist eine humangenetische Abklärung zum Test einer PTH1-Rezeptor-Mutation ein wichtiges diagnostisches Mittel, um nicht erfolgsversprechende kieferorthopädische Therapien zu vermeiden und Behandlungsalternativen planen zu können.
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10

Zhang, Yan-Liang, John A. Frangos, and Mirianas Chachisvilis. "Mechanical stimulus alters conformation of type 1 parathyroid hormone receptor in bone cells." American Journal of Physiology-Cell Physiology 296, no. 6 (June 2009): C1391—C1399. http://dx.doi.org/10.1152/ajpcell.00549.2008.

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Анотація:
The molecular mechanisms by which bone cells transduce mechanical stimuli into intracellular biochemical responses have yet to be established. There is evidence that mechanical stimulation acts synergistically with parathyroid hormone PTH(1-34) in mediating bone growth. Using picosecond time-resolved fluorescence microscopy and G protein-coupled receptor conformation-sensitive fluorescence resonance energy transfer (FRET), we investigated conformational transitions in parathyroid hormone type 1 receptor (PTH1R). 1) A genetically engineered PTH1R sensor containing an intramolecular FRET pair was constructed that enabled detection of conformational activity of PTH1R in single cells. 2) The nature of ligand-dependent conformational change of PTH1R depends on the type of ligand: stimulation with the PTH(1-34) leads to conformational transitions characterized by decrease in FRET efficiency while NH2-terminal truncated ligand PTH(3-34) stimulates conformational transitions characterized by higher FRET efficiencies. 3) Stimulation of murine preosteoblastic cells (MC3T3-E1) with fluid shear stress (FSS) leads to significant changes in conformational equilibrium of the PTH1R in MC3T3-E1 cells, suggesting that mechanical perturbation of the plasma membrane leads to ligand-independent response of the PTH1R. Conformational transitions induced by mechanical stress were characterized by an increase in FRET efficiency, similar to those induced by the NH2-terminal truncated ligand PTH(3-34). The response to the FSS stimulation was inhibited in the presence of PTH(1-34) in the flow medium. These results indicate that the FSS can modulate the action of the PTH(1-34) ligand. 4) Plasma membrane fluidization using benzyl alcohol or cholesterol extraction also leads to conformational transitions characterized by increased FRET levels. We therefore suggest that PTH1R is involved in mediating primary mechanochemical signal transduction in MC3T3-E1 cells.
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Більше джерел

Дисертації з теми "Parathyroid Hormone Receptor (PTH1R)"

1

Kwan, Mei Yee. "Transcription regulation of murine parathyroid hormone/parathyroid hormone related peptide receptor (PTH1R)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0030/MQ64385.pdf.

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2

Kwan, Mei Yee 1971. "Transcription regulation of murine parathyroid hormoneparathyroid hormone related peptide receptor (PTH1R)." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=30681.

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Our first aim was to generate transgenic mice to express beta-galactosidase reporter gene under the control of the two promoters. The model would allow us to study the temporal and spatial expression of PTH1R during the onset of embryonic endochondral ossification, and in the adult. Our transgenic animals would allow us to identify regulatory elements that are essential for tissue specific PTH1R expression. We have cloned 11 kilobases of mouse PTH1R gene promoter sequence containing four untranslated exons U1, U2, U3 and SS, and fused this to a Lac Z reporter gene, which was in turn fused to a 250 by fragment containing the A-rich polyadenylylation signal. Three additional constructs were made with deletion of transcription start sites in exon U1 (DeltaU1), U3 (DeltaU3) and both (DeltaU1DeltaU3). Both the control and transgenic adult littermates showed high levels of beta-galactosidase-like activity in epiphyseal growth plate and kidney medulla. However, beta-galactosidase activity was not observed for fetuses aged post coital 14.5 and 15.5 days. We were unable to show tissue specific reporter activity in our transgenic animals.
In other study, we found that P2 is the predominant promoter controlling PTH1R gene expression in both bone and cartilage. (Abstract shortened by UMI.)
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3

Panda, Dibyendu. "Role of Tuberoinfundibular peptide 39 (TIP 39)/ parathyroid hormone 2 receptor (PTH2R) signalling in the control of endochondral bone formation." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104517.

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Анотація:
Parathyroid hormone (PTH) family members participate actively in various steps of endochondral bone development, in maintenance of bone health, and in mineral homeostasis. PTH type 2 receptor (PTH2R) and its ligand tuberoinfundibular peptide of 39 residues (TIP39) are recent additions to the PTH family of receptors and ligands. They are abundantly expressed in brain where it is proposed to possess neurotransmitter function.In this study, we demonstrate the presence of both TIP39 and PTH2R in the growth plate of murine long bones, and we show that the periarticular chondrocytes which express PTH2R are spatially separated from the hypertrophic chondrocytes expressing TIP39. Using CFK2 chondrocytic cells as an in vitro model, we demonstrate that TIP39/PTH2R signalling impairs cell proliferation through inhibition of progression at the G0/G1 phase of the cell cycle. We also show that this signalling inhibits cell differentiation through deregulated expression of the master transcription factor of chondrocyte function, Sox9.In order to investigate the in vivo functions of the TIP39/PTH2R signalling pathway, we generated transgenic mice overexpressing PTH2R in chondrocytes under the control of the Collagen type II promoter/enhancer. We observed that PTH2R overexpression reduced chondrocyte proliferation and impaired trabecular bone formation likely through alterations in Wnt signalling and β-catenin expression. In addition, PTH2R overexpression was observed to delay growth plate secondary ossification in postnatal development, thus retarding endochondral bone growth. We further observed a downregulation of GDF5, a member of the bone morphogeneticprotein family, and of WDR5, a transcriptional modulator of articular chondrocytes, two factors previously shown to influence the development of the secondary ossification centre.Taken together, our results indicate that TIP39 and PTH2R in growth plate chondrocytes exert a crucial signalling role during endochondral bone development. Further studies are needed to explore these functions in experimental pathological models such as chondrodysplasias and possibly osteoarthritis.
Les membres de la famille de l'hormone parathyroïdienne (PTH) participent au développement de l'os endochondral, et au maintien de la santé osseuse et de l'homéostasie minérale. Le récepteur de type 2 de la PTH (PTH2R), et son ligand le peptide tubéroinfundibulaire de 39 acides aminés (TIP39) sont des nouveaux membres de la famille des récepteurs de la PTH et ses ligands. Ils sont exprimés en abondance dans le cerveau où on leur attribue des fonctions de neurotransmetteurs.Dans la présente étude, nous démontrons chez la souris la présence du TIP39 et du PTH2R dans la plaque de croissance des os longs, et nous mettons en évidence la séparation spatiale des chondrocytes périarticulaires exprimant le PTH2R, et des chondrocytes hypertrophiques exprimant le TIP39. A l'aide du modèle in vitro de cellules chondrocytiques CFK2, nous démontrons que la signalisation du complexe TIP39/PTH2R ralentit la prolifération cellulaire en inhibant la progression au delà de la phase G0/G1 du cycle cellulaire. De plus, nous demontrons que la différenciation cellulaire est inhibée par la dérégulation de l'expression du Sox9, le principal facteur de transcription contrôlant la fonction chondrocytaire.Afin d'évaluer les fonctions in vivo de la voie de signalisation du complexe TIP39/PTH2R, nous avons géneré des souris transgéniques surexprimant le PTH2R dans les chondrocytes sous le contrôle du promoteur du gène du Collagène de type II. La surexpression du PTH2R a réduit la prolifération des chondrocytes et inhibé la formation de l'os trabéculaire, probablement par une modification de la signalisation du Wnt et de l'expression de la β-caténine. De plus, durant le développement post-natal, la surexpression du PTH2R a ralenti l'ossification de la plaque de croissancesecondaire, retardant ainsi la croissance de l'os endochondral. Nous avons de plus observé une diminution de l'activité de GDF5 et de WDR5 (respectivement membre de la famille des protéines morphogéniques de l'os, et modulateur transcriptionel des chondrocytes articulaires), deux facteurs connus pour influencer le développement du centre d'ossification secondaire.En conclusion, nos résultats indiquent que le TIP39 et le PTH2R jouent un rôle crucial de signalisation au cours du développement de l'os endochondral. Des études futures sont nécessaires afin d'explorer les fonctions du TIP39 et du PTH2R dans divers modèles expérimentaux, dont ceux de la chondrodysplasie et possiblement dans l'ostéoarthrite.
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4

Bettoun, Joan David. "Studies on the transcriptional regulation and differential splicing of the human parathyroid hormone (PTH)/PTH-related peptide (PTHRP) receptor gene (PTHR)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0025/NQ50114.pdf.

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5

Alokail, Majed Saleh Abdullah. "Parathyroid hormone-related peptide and parathyroid hormone-related peptide receptor in breast cancer MCF7 cells." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297420.

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6

Weaver, Richard Emyr. "Ligand-receptor interactions at the parathyroid hormone receptors." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531595.

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7

Mitchell, Jane. "Characterization of parathyroid hormone receptor desensitization in vivo and in vitro." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74325.

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This thesis examines in vivo and in vitro the effects of prolonged exposure of target cells to PTH on PTH receptors and postreceptor components of the adenylate cyclase system. Using a vitamin D-deficient ($-$D) rat model, hyperparathyroidism in vivo resulted in a decreased number of PTH receptors in kidney and a decreased amount of G protein $ alpha$ subunits. The decreased amount of G$ sb{ rm s} alpha$ was shown to be specific for PTH target tissue and may have played a role in the heterologous desensitization of CT-stimulated adenylate cyclase, demonstrated in renal membranes from the $-$D rats. The study of the control of PTH receptors was pursued using an osteosarcoma clonal cell line, UMR-106, in vitro. Initial characterization of these cells revealed abundant, saturable, cell surface PTH receptors linked to the adenylate cyclase system. Demonstration that the majority of PTH binding was associated with morphologically distinct cells in the UMR-106 population indicated that PTH receptors may be maximally expressed during specific stages in the cell cycle. PTH receptors in UMR-106 cells were shown to be regulated by distinct homologous and heterologous mechanisms. PTH-mediated, homologous desensitization was associated with down-regulation of PTH receptors and loss of G$ sb{ rm s} alpha$ protein form the cell membrane. Heterologous desensitization of PTH responses by PGE$ sb2$ was shown to be cAMP mediated, resulting in a reversible modification of the PTH receptors. This work has demonstrated that multiple mechanisms exist for the regulation of PTH responses both in vivo and in vitro that involve modifications of both the PTH receptors and postreceptor components of the adenylate cyclase system.
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8

Nuersailike, Abuduwali [Verfasser]. "Characterization of Parathyroid Hormone 1 Receptor in Periodontal Ligament Cells / Abuduwali Nuersailike." Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/1044080973/34.

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9

Aghaloo, Tara Lyn. "Parathyroid hormone and 1a, 25-dihydroxyvitamin D3 regulation of the vitamin D receptor in osteoblasts." Diss., Restricted to subscribing institutions, 2007. http://proquest.umi.com/pqdweb?did=1320942021&sid=2&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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10

Sakwe, Amos M. "The Role of Protein Kinase C in the Extracellular Ca2+-regulated Secretion of Parathyroid Hormone." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4637.

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Parathyroid hormone (PTH) is the major physiological regulator of the extracellular Ca2+ concentration ([Ca2+]o) in the body. The secretion of this hormone is suppressed at high [Ca2+]o. Previously this was thought to occur by intracellular degradation of the hormone in the secretory pathway of parathyroid (PT) cells but is now believed to result from extracellular Ca2+ stimulus-secretion coupling via the calcium sensing receptor (CaR). In contrast to the stimulation of PTH secretion upon inhibition of mature PTH proteolysis, inhibition of PT proteasomes caused the accumulation of PTH precursors and inhibited secretion of PTH. This suggests that PT proteasomes play a quality control function in the maturation of PTH but they do not directly participate in the [Ca2+]o-regulated secretion of the hormone. Treatment of PT cells with 12-O-tetradecanyolphorbol-13-acetate (TPA) blocks the high [Ca2+]o-induced CaR-mediated suppression of PTH secretion. To delineate the role of DAG-responsive protein kinase C (PKC) isoforms in this process, we complemented pharmacological modulation of PKC activity with physiological activation of the enzyme via the CaR. PKC-α was rapidly activated by high [Ca2+]o and was efficiently down-regulated by prolonged TPA treatment. In CaR-transfected HEK293 cells, TPA and high [Ca2+]o induced the activation of ERK1/2 but the TPA effect was CaR- and Ca2+-independent. The magnitude of neomycin-induced release of Ca2+ from intracellular stores following pharmacological modulation of PKC activity was opposite to that resulting from physiological activation/inhibition of the enzyme via the CaR. Influx of Ca2+ following activation of the receptor occurred by store-operated mechanisms. Over-expression of wt or DN PKC-α or-ε in PT cells using the Tet-On adenovirus gene delivery system revealed that the stimulatory effect of TPA on PTH secretion at high [Ca2+]o was enhanced in cells over-expressing wt PKC-α, but the coupling of the extracellular Ca2+ signal to PTH secretion was not dependent on the physiological activation of this PKC isoform via the CaR.
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Книги з теми "Parathyroid Hormone Receptor (PTH1R)"

1

Mau, Elaine. Characterization of parathyroid hormone receptor-1 (PTHR1) signaling: The R150C mutation, found in cartilage neoplasia. 2004.

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2

Cheung, Ricky. Modulation of parathyroid hormone receptor signal transduction pathways in osteoblasts. 2005.

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3

Newell-Price, John, Alia Munir, and Miguel Debono. Primary hyperparathyroidism. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0187.

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Primary hyperparathyroidism is a disorder of bone mineralization and renal physiology due to excess parathyroid hormone secretion. Parathyroid hormone (PTH) is produced and released by the parathyroid chief cells, under regulation of the G- protein-coupled calcium-sensing receptor. Primary hyperparathyroidism occurs when there is a loss of the inhibitory feedback of PTH release by extracellular calcium. The rise in PTH levels is initially associated with a normal serum calcium, and then over time with hypercalcaemia. The most common cause of primary hyperparathyroidism is a benign solitary adenoma (80%). Other causes include multiple adenomas and hyperplasia. This chapter reviews the causes, clinical features, and management of primary hyperparathyroidism.
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4

Trepiccione, Francesco, and Giovambattista Capasso. Calcium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0026.

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Ca2+ homeostasis is achieved through a fine balance among three main organs: the intestine, the kidney, and bone. Blood levels of Ca2+ are accurately tuned through the Ca2+ sensing receptors and regulated by several hormones, including parathyroid hormone (PTH), active vitamin D, and calcitonin. The most recent findings in Ca2+ handling are described. The role of the Ca2+ sensing receptor, as well as Klotho, a new player participating in Ca2+ homeostasis, are described. Finally, the effects of diuretics, calcineurin inhibitors, and the link between hypertension and Ca2+ metabolism are reviewed.
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5

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
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Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

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Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.
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7

Elder, Grahame J. Metabolic bone disease after renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0288.

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Patients who undergo kidney transplantation have laboratory, bone, and soft tissue abnormalities that characterize chronic kidney disease mineral and bone disorder (CKD-MBD). After successful transplantation, abnormal values of parathyroid hormone, fibroblast growth factor 23, calcium, phosphate, vitamin D sterols, and sex hormones generally improve, but abnormalities often persist. Cardiovascular risk remains high and is influenced by prevalent vascular calcification, and fracture risk increases due to a combination of abnormal bone ‘quality’, compounded by immunosuppressive drugs and reductions in bone mineral density. Patients with well managed CKD-MBD before transplantation generally have a smoother post-transplant course, and it is useful to assess patients soon after transplantation for risk factors relevant to the general population and to patients with CKD. Targeted laboratory assessment, bone densitometry, and X-ray of the spine are useful for guiding therapy to minimize post-transplant effects of CKD-MBD. To reduce fracture risk, general measures include glucocorticoid dose minimization, attaining adequate 25(OH)D levels, and maintaining calcium and phosphate values in the normal range. Calcitriol or its analogues and antiresorptive agents such as bisphosphonates may protect bone from glucocorticoid effects and ongoing hyperparathyroidism, but the efficacy of these therapies to reduce fractures is unproven. Alternate therapies with fewer data include denosumab, strontium ranelate, teriparatide, oestrogen or testosterone hormone replacement therapy, tibolone, selective oestrogen receptor modulators, and cinacalcet. Parathyroidectomy may be necessary, but is generally avoided within the first post-transplant year. A schema is presented in this chapter that aims to minimize harm when allocating therapy.
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Частини книг з теми "Parathyroid Hormone Receptor (PTH1R)"

1

Kopp, Peter. "Parathyroid Hormone Receptor." In Endocrine Pathology, 625–26. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5175.

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2

Kopp, Peter. "Parathyroid Hormone Receptor." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-28845-1_5175-1.

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3

Suva, L. J. "Novel Aspects of Parathyroid Hormone/Parathyroid Hormone-Related Protein Hormone-Receptor Interactions." In Novel Approaches to Treatment of Osteoporosis, 211–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-09007-7_10.

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4

Gardella, Thomas J. "The Parathyroid Hormone Receptor Type 1." In Osteoporosis, 323–47. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-69287-6_16.

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5

Kawashima, Hiroyuki. "1, 25-Dihydroxyvitamin D Receptor and its Biological Role in Vascular Smooth Muscle Cell Functions." In New Actions of Parathyroid Hormone, 109–12. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0567-5_14.

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6

Nissenson, Robert A., Elaina Mann, Jane Winer, Anne Teitelbaum, and Claude D. Arnaud. "Solubilization of a Guanine Nucleotide-Sensitive Parathyroid Hormone-Receptor Complex from Canine Renal Cortex." In Phosphate and Mineral Homeostasis, 329–43. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_41.

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Chorev, M., V. Behar, C. Nakamoto, A. E. Adams, S. M. Stueckle, L. J. Suva, and M. Rosenblatt. "Benzophenone-modified parathyroid hormone (PTH) analogs as novel tools for ‘photoaffinity scanning’ of ligand-receptor interactions." In Peptides 1994, 125–26. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-1468-4_46.

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8

Hruska, Keith, Robert Dunlay, Roberto Civitelli, Akimitsu Miyauchi, Constanta Victoriea Dobre, and Ajay Gupta. "Parathyroid Hormone Receptor Coupling to Phospholipase C is an Alternate Pathway of Signal Transduction in the Bone and Kidney." In Nephrology, 1499–508. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_156.

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9

Goltzman, David, and Geoffrey N. Hendy. "Parathyroid Anatomy, Hormone Synthesis, Secretion, Action, and Receptors." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 631–40. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0081.

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Parathyroid hormone (PTH) is produced in the parathyroid glands and is released as an 84 amino acid polypeptide whose bioactivity resides in its amino-terminal domain. PTH secretion is controlled by the parathyroid calcium-sensing receptor (CaSR), and inactivating or activating mutations in this receptor lead to inherited hypercalcaemic and hypocalcaemic disorders, respectively. PTH regulates extracellular fluid calcium homeostasis through its renal calcium-conserving action, and its bone resorbing actions. Adenomas or hyperplasia of the parathyroid glands can lead to dysregulated PTH secretion and the disorder hyperparathyroidism. Intermittently administered PTH, however, exerts a bone anabolic effect and has found use in the clinic in the treatment of osteoporosis. Both PTH (and the gene family member, parathyroid hormone-related protein or PTHrP) act through a G-protein-coupled receptor, the type 1 PTH/PTHrP receptor (PTHR1) that is widely expressed and signals through multiple second messenger pathways. Inactivating mutations in the PTHR1 cause Blomstrand’s lethal chondrodysplasia, whereas activating mutations are found in Jansen’s metaphyseal chondrodysplasia.
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Zhang, Xiaoying, Nagesha K. Guthalu, Katoura Williams, Anaïs Mozar, and Vasavada Rupangi. "Physiological Role of Parathyroid Hormone-Related Protein (PTHrP) and Parathyroid Hormone-1 Receptor (PTH1R) Signaling in the Pancreatic β-Cell." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–116—P1–116. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p3.p1-116.

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Тези доповідей конференцій з теми "Parathyroid Hormone Receptor (PTH1R)"

1

Hastings, Randolph H., Ryan Vander Werff, Philippe R. Montgrain, and Rick Quintana. "Parathyroid Hormone-Related Protein (PTHrP) Inhibits Lung Cancer Proliferation Through The Classic PTHrP Receptor." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5080.

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Звіти організацій з теми "Parathyroid Hormone Receptor (PTH1R)"

1

Leach, Roland M., Carol V. Gay, Mark Pines, and Shmuel Hurwitz. Developing Nutritional-Management Protocols which Prevent Tibial Dyschondroplasia. United States Department of Agriculture, September 1996. http://dx.doi.org/10.32747/1996.7573994.bard.

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The objectives of this proposal were (1) to develop early age short-term restrict feeding protocols which eliminate the incidence of TD without compromising market weight performance and (2) monitor the components of the PTH/PTHrP cascade in conjunction with the development of the protocols in Objective 1. In this investigation it was established that changes in gene expression associated with TD occur as early as 13 days of age. This means that management strategies for the control of this disease must be established during the initial two weeks of rearing. In order to determine a focus for these management strategies, attempts were made to identify the metabolic defect responsible for tibial dyschondroplasia. Therefore, the parathyroid hormone/parathyrod related peptide (PTH/PTHrP) cascade of events was investigated. This emphasis was based on the fact that many nutritional factors that influence TD could be operating through this system. Secondly, the receptor for these peptides acts as the gatekeeper of chondrocyte differentiation. Examination of many aspects of this cascade led to the conclusion that TD is not the direct result of perturbation of this PTH/PTHrP receptor but is likely to develop from an interruption of a pathway downstream from this receptor.
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