Source:http://linkedlifedata.com/resource/pubmed/id/11747990
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2001-12-18
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pubmed:abstractText |
In PC-Cl3 rat thyroid cell line, ATP and UTP provoked a transient increase in [Ca(2+)](i), followed by a lower sustained phase. Removal of extracellular Ca(2+) reduced the initial transient response and completely abolished the plateau phase. Thapsigargin (TG) caused a rapid rise in [Ca(2+)](i) and subsequent addition of ATP was without effect. The transitory activation of [Ca(2+)](i) was dose-dependently attenuated in cells pretreated with the specific inhibitor of phospholipase C (PLC), U73122. These data suggest that the ATP-stimulated increment of [Ca(2+)](i) required InsP(3) formation and binding to its specific receptors in Ca(2+) stores. Desensitisation was demonstrated with respect to the calcium response to ATP and UTP in Fura 2-loaded cells. Further studies were performed to investigate whether the effect of ATP on Ca(2+) entry into PC-Cl3 cells was via L-type voltage-dependent Ca(2+) channels (L-VDCC) and/or by the capacitative pathway. Nifedipine decreased ATP-induced increase on [Ca(2+)](i). Addition of 2 mM Ca(2+) induced a [Ca(2+)](i) rise after pretreatment of the cells with TG or with 100 microM ATP in Ca(2+)-free medium. These data indicate that Ca(2+) entry into PC-Cl3 stimulated with ATP occurs through both an L-VDCC and through a capacitative pathway. Using buffers with differing Na(+) concentrations, we found that the effects of ATP were dependent of extracellular Na(+), suggesting that a Na(+)/Ca(2+) exchange mechanism is also operative. These data suggest the existence, in PC-Cl3 cell line, of a P2Y purinergic receptor able to increase the [Ca(2+)](i) via PLC activation, Ca(2+) store depletion, capacitative Ca(2+) entry and L-VDCC activation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-(6-((3-methoxyestra-1,3,5(10)-trie...,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Estrenes,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrrolidinones,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Purinergic P2,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases,
http://linkedlifedata.com/resource/pubmed/chemical/Uridine Triphosphate
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0898-6568
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
61-7
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11747990-Adenosine Triphosphate,
pubmed-meshheading:11747990-Animals,
pubmed-meshheading:11747990-Calcium,
pubmed-meshheading:11747990-Calcium Channel Blockers,
pubmed-meshheading:11747990-Calcium Channels, L-Type,
pubmed-meshheading:11747990-Calcium Signaling,
pubmed-meshheading:11747990-Cell Line,
pubmed-meshheading:11747990-Dose-Response Relationship, Drug,
pubmed-meshheading:11747990-Enzyme Inhibitors,
pubmed-meshheading:11747990-Estrenes,
pubmed-meshheading:11747990-Kinetics,
pubmed-meshheading:11747990-Nifedipine,
pubmed-meshheading:11747990-Pyrrolidinones,
pubmed-meshheading:11747990-Rats,
pubmed-meshheading:11747990-Receptors, Purinergic P2,
pubmed-meshheading:11747990-Sodium,
pubmed-meshheading:11747990-Thyroid Gland,
pubmed-meshheading:11747990-Type C Phospholipases,
pubmed-meshheading:11747990-Uridine Triphosphate
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pubmed:year |
2002
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pubmed:articleTitle |
Increase of [Ca(2+)](i) via activation of ATP receptors in PC-Cl3 rat thyroid cell line.
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pubmed:affiliation |
Laboratory of Physiology, Department of Biology, University of Lecce, Lecce 73100, Italy. smarsi@ilenic.unile.it
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pubmed:publicationType |
Journal Article
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