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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0023602,
umls-concept:C0026336,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0035647,
umls-concept:C0035820,
umls-concept:C0036536,
umls-concept:C0036537,
umls-concept:C0070099,
umls-concept:C0149911,
umls-concept:C0185117,
umls-concept:C0249742,
umls-concept:C0521119,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2000-4-19
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pubmed:abstractText |
Humoral hypercalcemia of malignancy (HHM) occurs when secretion of parathyroid hormone-related peptide (PTHrP) by cancer cells causes hypercalcemia in the absence of skeletal metastases. High extracellular calcium (Ca(2+)(o)) increases secretion of PTH-like bioactivity by rat H-500 leydig cells, a transplantable model of HHM, an action potentially mediated by the Ca(2+)(o)-sensing receptor (CaR). In this study we investigated whether H-500 cells express the CaR and, if so, whether CaR agonists modulate PTHrP secretion. Northern blot analysis and RT-PCR revealed bona fide CaR transcript(s), and immunocytochemistry and Western analysis with a specific anti-CaR antiserum demonstrated CaR protein expression in H-500 cells. Furthermore, high Ca(2+)(o) and neomycin stimulated PTHrP secretion dose-dependently with maximal 2.7- and 3.3-fold increases at 5 mM Ca(2+)(o) and 300 microM neomycin, respectively. Thus in HHM caused by H-500 cells, the CaR could participate in a vicious cycle whereby PTHrP-induced increases in Ca(2+)(o) further stimulate PTHrP release and exacerbate hypercalcemia.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0006-291X
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2000 Academic Press.
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pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
269
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
427-32
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10708570-Animals,
pubmed-meshheading:10708570-Blotting, Northern,
pubmed-meshheading:10708570-Blotting, Western,
pubmed-meshheading:10708570-Extracellular Space,
pubmed-meshheading:10708570-Hypercalcemia,
pubmed-meshheading:10708570-Immunohistochemistry,
pubmed-meshheading:10708570-Leydig Cells,
pubmed-meshheading:10708570-Male,
pubmed-meshheading:10708570-Models, Biological,
pubmed-meshheading:10708570-Neoplasms, Experimental,
pubmed-meshheading:10708570-Parathyroid Hormone-Related Protein,
pubmed-meshheading:10708570-Proteins,
pubmed-meshheading:10708570-RNA, Messenger,
pubmed-meshheading:10708570-Rats,
pubmed-meshheading:10708570-Rats, Inbred F344,
pubmed-meshheading:10708570-Receptors, Calcium-Sensing,
pubmed-meshheading:10708570-Receptors, Cell Surface,
pubmed-meshheading:10708570-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
2000
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pubmed:articleTitle |
Extracellular calcium-sensing receptor (CaR) expression and its potential role in parathyroid hormone-related peptide (PTHrP) secretion in the H-500 rat Leydig cell model of humoral hypercalcemia of malignancy.
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pubmed:affiliation |
Endocrine-Hypertension Division, Harvard Medical School, Boston, Massachusetts, 02115, USA. jsanders@rics.bwh.harvard.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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