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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
Pt 3
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pubmed:dateCreated |
2001-2-22
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pubmed:abstractText |
The regulation of organelle free Ca2+ was analysed in individual mouse pancreatic beta-cells loaded with the fluorescent low-affinity indicator furaptra. Removal of the cytoplasmic indicator by controlled digitonin permeabilization of the plasma membrane resulted in a sudden increase of the 340 nm/380 nm fluorescence excitation ratio followed by a gradual decay, reflecting the emptying of Ca2+ from organelle pools. Subsequent introduction of 3 mM ATP caused rapid refilling of a Ca2+ pool, which represented the endoplasmic reticulum (ER) in being mobilized with inositol 1,4,5-trisphosphate (IP3) and the sarco(endo)plasmic reticulum Ca2+-ATPase inhibitor thapsigargin. The concentration of Ca2+ in the ER observed immediately after permeabilization depended on the glucose concentration in a hyperbolic fashion with half-maximal filling at about 6 mM of the sugar. Glucose promotion of Ca2+ sequestration in the ER involved a high-affinity mechanism not requiring but accelerated by a rise of the cytoplasmic Ca2+ concentration. Glucose also exerted a long-term action on the ER storage of Ca2+, maintaining the set-point for its maximal concentration and preserving the response to IP3. The results indicate that the ER has an important role in the glucose-stimulated beta-cell by serving as a high-affinity sink for Ca2+, irrespective of the prevailing concentration of cytoplasmic Ca2+.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11158282-10070018,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11158282-10212237,
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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 |
Feb
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
530
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
533-40
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11158282-Adenosine Triphosphate,
pubmed-meshheading:11158282-Animals,
pubmed-meshheading:11158282-Biological Transport,
pubmed-meshheading:11158282-Calcium,
pubmed-meshheading:11158282-Cells, Cultured,
pubmed-meshheading:11158282-Endoplasmic Reticulum,
pubmed-meshheading:11158282-Fluorescent Dyes,
pubmed-meshheading:11158282-Fura-2,
pubmed-meshheading:11158282-Glucose,
pubmed-meshheading:11158282-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:11158282-Islets of Langerhans,
pubmed-meshheading:11158282-Kinetics,
pubmed-meshheading:11158282-Mice,
pubmed-meshheading:11158282-Mice, Obese,
pubmed-meshheading:11158282-Organelles,
pubmed-meshheading:11158282-Thapsigargin
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pubmed:year |
2001
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pubmed:articleTitle |
The endoplasmic reticulum is a glucose-modulated high-affinity sink for Ca2+ in mouse pancreatic beta-cells.
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pubmed:affiliation |
Department of Medical Cell Biology, Uppsala University, Biomedical Centre, Box 571, SE-751 23 Uppsala, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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