Source:http://linkedlifedata.com/resource/pubmed/id/12887971
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2003-7-30
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| pubmed:abstractText |
Liver cells possess store-operated Ca2+ channels (SOCs) with a high selectivity for Ca2+ compared with Na+, and several types of intracellular messenger-activated non-selective cation channels with a lower selectivity for Ca2+ (NSCCs). The main role of SOCs is thought to be in refilling depleted endoplasmic reticulum Ca2+ stores [Cell Calcium 7 (1986) 1]. NSCCs may be involved in refilling intracellular stores but are also thought to have other roles in regulating the cytoplasmic-free Ca2+ and Na+ concentrations. The ability of SOCs to refill the endoplasmic reticulum Ca2+ stores in hepatocytes has not previously been compared with that of NSCCs. The aim of the present studies was to compare the ability of SOCs and maitotoxin-activated NSCCs to refill the endoplasmic reticulum in rat hepatocytes. The experiments were performed using fura-2FF and fura-2 to monitor the free Ca2+ concentrations in the endoplasmic reticulum and cytoplasmic space, respectively, a Ca2+ add-back protocol, and 2-aminoethyl diphenylborate (2-APB) to inhibit Ca2+ inflow through SOCs. In cells treated with 2,5-di-t-butylhydroquinone (DBHQ) or vasopressin to deplete the endoplasmic reticulum Ca2+ stores, then washed to remove DBHQ or vasopressin, the addition of Ca2+ caused a substantial increase in the concentration of Ca2+ in the endoplasmic reticulum and cytoplasmic space due to the activation of SOCs. These increases were inhibited 80% by 2-APB, indicating that Ca2+ inflow is predominantly through SOCs. In the presence of 2-APB (to block SOCs), maitotoxin induced a substantial increase in [Ca2+](cyt), but only a modest and slower increase in [Ca2+](er). Under these conditions, Ca2+ inflow is predominantly through maitotoxin-activated NSCCs. It is concluded that SOCs are more effective than maitotoxin-activated NSCCs in refilling the endoplasmic reticulum Ca2+ stores. The previously developed concept of a specific role for SOCs in refilling the endoplasmic reticulum is consistent with the results reported here.
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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/2,5-di-tert-butylhydroquinone,
http://linkedlifedata.com/resource/pubmed/chemical/Boron Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Ca(2 ) Mg(2 )-ATPase,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Epinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroquinones,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Marine Toxins,
http://linkedlifedata.com/resource/pubmed/chemical/Oxocins,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin,
http://linkedlifedata.com/resource/pubmed/chemical/Vasopressins,
http://linkedlifedata.com/resource/pubmed/chemical/maitotoxin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
0143-4160
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
34
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
241-51
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12887971-Animals,
pubmed-meshheading:12887971-Boron Compounds,
pubmed-meshheading:12887971-Ca(2+) Mg(2+)-ATPase,
pubmed-meshheading:12887971-Calcium,
pubmed-meshheading:12887971-Calcium Channel Agonists,
pubmed-meshheading:12887971-Calcium Channel Blockers,
pubmed-meshheading:12887971-Calcium Channels,
pubmed-meshheading:12887971-Cytoplasm,
pubmed-meshheading:12887971-Endoplasmic Reticulum,
pubmed-meshheading:12887971-Epinephrine,
pubmed-meshheading:12887971-Fura-2,
pubmed-meshheading:12887971-Hepatocytes,
pubmed-meshheading:12887971-Hydroquinones,
pubmed-meshheading:12887971-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:12887971-Ion Channels,
pubmed-meshheading:12887971-Kinetics,
pubmed-meshheading:12887971-Male,
pubmed-meshheading:12887971-Marine Toxins,
pubmed-meshheading:12887971-Microscopy, Fluorescence,
pubmed-meshheading:12887971-Oxocins,
pubmed-meshheading:12887971-Rats,
pubmed-meshheading:12887971-Rats, Wistar,
pubmed-meshheading:12887971-Thapsigargin,
pubmed-meshheading:12887971-Vasopressins
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| pubmed:year |
2003
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| pubmed:articleTitle |
Evidence that store-operated Ca2+ channels are more effective than intracellular messenger-activated non-selective cation channels in refilling rat hepatocyte intracellular Ca2+ stores.
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| pubmed:affiliation |
Department of Medical Biochemistry, School of Medicine, Faculty of Health Sciences, Flinders University, G.P.O. Box 2100, South Australia 5001, Adelaide, Australia.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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