PoplarV1, Main, Exploration, bibRecord, 000785

Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion.

Identifieur interne : 000785 ( Main/Exploration ); précédent : 000784; suivant : 000786

Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion.

Auteurs : Patricia P. Centeno [Royaume-Uni] ; Amanda Herberger [États-Unis] ; Hee-Chang Mun [Australie] ; Chialing Tu [États-Unis] ; Edward F. Nemeth [Canada] ; Wenhan Chang [États-Unis] ; Arthur D. Conigrave [Australie] ; Donald T. Ward [Royaume-Uni]

Source :

Nature communications [ 2041-1723 ] ; 2019.

RBID : pubmed:31619668

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Gene Knockout Techniques (MeSH), HEK293 Cells (MeSH), Humans (MeSH), Hyperparathyroidism, Secondary (etiology), Hyperparathyroidism, Secondary (metabolism), Mice (MeSH), Mutation (MeSH), Parathyroid Glands (metabolism), Parathyroid Hormone (metabolism), Phosphates (metabolism), Receptors, Calcium-Sensing (genetics), Receptors, Calcium-Sensing (metabolism), Renal Insufficiency, Chronic (complications), Renal Insufficiency, Chronic (metabolism).
MESH :
- chemical , genetics : Receptors, Calcium-Sensing.
- chemical , metabolism : Parathyroid Hormone, Phosphates, Receptors, Calcium-Sensing.
- complications : Renal Insufficiency, Chronic.
- etiology : Hyperparathyroidism, Secondary.
- metabolism : Hyperparathyroidism, Secondary, Parathyroid Glands, Renal Insufficiency, Chronic.
- Animals, Gene Knockout Techniques, HEK293 Cells, Humans, Mice, Mutation.

Abstract

Extracellular phosphate regulates its own renal excretion by eliciting concentration-dependent secretion of parathyroid hormone (PTH). However, the phosphate-sensing mechanism remains unknown and requires elucidation for understanding the aetiology of secondary hyperparathyroidism in chronic kidney disease (CKD). The calcium-sensing receptor (CaSR) is the main controller of PTH secretion and here we show that raising phosphate concentration within the pathophysiologic range for CKD significantly inhibits CaSR activity via non-competitive antagonism. Mutation of residue R62 in anion binding site-1 abolishes phosphate-induced inhibition of CaSR. Further, pathophysiologic phosphate concentrations elicit rapid and reversible increases in PTH secretion from freshly-isolated human parathyroid cells consistent with a receptor-mediated action. The same effect is seen in wild-type murine parathyroid glands, but not in CaSR knockout glands. By sensing moderate changes in extracellular phosphate concentration, the CaSR represents a phosphate sensor in the parathyroid gland, explaining the stimulatory effect of phosphate on PTH secretion.

DOI: 10.1038/s41467-019-12399-9
PubMed: 31619668
PubMed Central: PMC6795806

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000661
to stream Main, to step Curation: 000661

Le document en format XML

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<term>Gene Knockout Techniques (MeSH)</term>
<term>HEK293 Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Hyperparathyroidism, Secondary (etiology)</term>
<term>Hyperparathyroidism, Secondary (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Parathyroid Glands (metabolism)</term>
<term>Parathyroid Hormone (metabolism)</term>
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<term>Hormone parathyroïdienne (métabolisme)</term>
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<term>Insuffisance rénale chronique (complications)</term>
<term>Insuffisance rénale chronique (métabolisme)</term>
<term>Mutation (MeSH)</term>
<term>Phosphates (métabolisme)</term>
<term>Récepteurs-détecteurs du calcium (génétique)</term>
<term>Récepteurs-détecteurs du calcium (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Techniques de knock-out de gènes (MeSH)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Parathyroid Hormone</term>
<term>Phosphates</term>
<term>Receptors, Calcium-Sensing</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Renal Insufficiency, Chronic</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Hyperparathyroidism, Secondary</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Insuffisance rénale chronique</term>
<term>Récepteurs-détecteurs du calcium</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hyperparathyroidism, Secondary</term>
<term>Parathyroid Glands</term>
<term>Renal Insufficiency, Chronic</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glandes parathyroïdes</term>
<term>Hormone parathyroïdienne</term>
<term>Hyperparathyroïdie secondaire</term>
<term>Insuffisance rénale chronique</term>
<term>Phosphates</term>
<term>Récepteurs-détecteurs du calcium</term>
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<term>Gene Knockout Techniques</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Mice</term>
<term>Mutation</term>
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<term>Cellules HEK293</term>
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<front><div type="abstract" xml:lang="en">Extracellular phosphate regulates its own renal excretion by eliciting concentration-dependent secretion of parathyroid hormone (PTH). However, the phosphate-sensing mechanism remains unknown and requires elucidation for understanding the aetiology of secondary hyperparathyroidism in chronic kidney disease (CKD). The calcium-sensing receptor (CaSR) is the main controller of PTH secretion and here we show that raising phosphate concentration within the pathophysiologic range for CKD significantly inhibits CaSR activity via non-competitive antagonism. Mutation of residue R62 in anion binding site-1 abolishes phosphate-induced inhibition of CaSR. Further, pathophysiologic phosphate concentrations elicit rapid and reversible increases in PTH secretion from freshly-isolated human parathyroid cells consistent with a receptor-mediated action. The same effect is seen in wild-type murine parathyroid glands, but not in CaSR knockout glands. By sensing moderate changes in extracellular phosphate concentration, the CaSR represents a phosphate sensor in the parathyroid gland, explaining the stimulatory effect of phosphate on PTH secretion.</div>
</front>
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<Abstract><AbstractText>Extracellular phosphate regulates its own renal excretion by eliciting concentration-dependent secretion of parathyroid hormone (PTH). However, the phosphate-sensing mechanism remains unknown and requires elucidation for understanding the aetiology of secondary hyperparathyroidism in chronic kidney disease (CKD). The calcium-sensing receptor (CaSR) is the main controller of PTH secretion and here we show that raising phosphate concentration within the pathophysiologic range for CKD significantly inhibits CaSR activity via non-competitive antagonism. Mutation of residue R62 in anion binding site-1 abolishes phosphate-induced inhibition of CaSR. Further, pathophysiologic phosphate concentrations elicit rapid and reversible increases in PTH secretion from freshly-isolated human parathyroid cells consistent with a receptor-mediated action. The same effect is seen in wild-type murine parathyroid glands, but not in CaSR knockout glands. By sensing moderate changes in extracellular phosphate concentration, the CaSR represents a phosphate sensor in the parathyroid gland, explaining the stimulatory effect of phosphate on PTH secretion.</AbstractText>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C095550">CASR protein, human</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<NameOfSubstance UI="D010281">Parathyroid Hormone</NameOfSubstance>
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Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion.

Phosphate acts directly on the calcium-sensing receptor to stimulate parathyroid hormone secretion.

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