Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-12-18
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
61-7
pubmed:dateRevised
2007-11-15
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
pubmed:year
2002
pubmed:articleTitle
Increase of [Ca(2+)](i) via activation of ATP receptors in PC-Cl3 rat thyroid cell line.
pubmed:affiliation
Laboratory of Physiology, Department of Biology, University of Lecce, Lecce 73100, Italy. smarsi@ilenic.unile.it
pubmed:publicationType
Journal Article