Source:http://linkedlifedata.com/resource/pubmed/id/18089647
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rdf:type | |
lifeskim:mentions |
umls-concept:C0030685,
umls-concept:C0040704,
umls-concept:C0079281,
umls-concept:C0391871,
umls-concept:C0521447,
umls-concept:C0596235,
umls-concept:C0680255,
umls-concept:C0687129,
umls-concept:C1283071,
umls-concept:C1516518,
umls-concept:C1698986,
umls-concept:C1963578,
umls-concept:C2334101,
umls-concept:C2349975
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pubmed:issue |
Pt 2
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pubmed:dateCreated |
2008-1-11
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pubmed:abstractText |
Nuclear Ca2+ plays a key role in the regulation of gene expression. Inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3)] might be an important regulator of nuclear Ca2+ but its contribution to nuclear Ca2+ signalling in adult cardiomyocytes remains elusive. We tested the hypothesis that endothelin-1 enhances nuclear Ca2+ concentration transients (CaTs) in rabbit atrial myocytes through Ins(1,4,5)P3-induced Ca(2+) release from perinuclear stores. Cytoplasmic and nuclear CaTs were measured simultaneously in electrically stimulated atrial myocytes using confocal Ca2+ imaging. Nuclear CaTs were significantly slower than cytoplasmic CaTs, indicative of compartmentalisation of intracellular Ca2+ signalling. Endothelin-1 elicited a preferential (10 nM) or a selective (0.1 nM) increase in nuclear versus cytoplasmic CaTs. This effect was abolished by inhibition of endothelin-1 receptors, phospholipase C and Ins(1,4,5)P3 receptors. Fractional Ca2+ release from the sarcoplasmic reticulum and perinuclear stores was increased by endothelin-1 at an otherwise unaltered Ca2+ load. Comparable increases of cytoplasmic CaTs induced by beta-adrenoceptor stimulation or elevation of extracellular Ca2+ could not mimic the endothelin-1 effects on nuclear CaTs, suggesting that endothelin-1 specifically modulates nuclear Ca2+ signalling. Thus, endothelin-1 enhances nuclear CaTs in atrial myocytes by increasing fractional Ca2+ release from perinuclear stores. This effect is mediated by the coupling of endothelin receptor A to PLC-Ins(1,4,5)P3 signalling and might contribute to excitation-transcription coupling.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0021-9533
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
121
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
186-95
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pubmed:meshHeading |
pubmed-meshheading:18089647-Animals,
pubmed-meshheading:18089647-Calcium,
pubmed-meshheading:18089647-Calcium Signaling,
pubmed-meshheading:18089647-Cell Nucleus,
pubmed-meshheading:18089647-Cytoplasm,
pubmed-meshheading:18089647-Endothelin-1,
pubmed-meshheading:18089647-Heart Atria,
pubmed-meshheading:18089647-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:18089647-Inositol 1,4,5-Trisphosphate Receptors,
pubmed-meshheading:18089647-Kinetics,
pubmed-meshheading:18089647-Microscopy, Confocal,
pubmed-meshheading:18089647-Models, Biological,
pubmed-meshheading:18089647-Muscle Cells,
pubmed-meshheading:18089647-Rabbits,
pubmed-meshheading:18089647-Sarcoplasmic Reticulum
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pubmed:year |
2008
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pubmed:articleTitle |
Endothelin-1 enhances nuclear Ca2+ transients in atrial myocytes through Ins(1,4,5)P3-dependent Ca2+ release from perinuclear Ca2+ stores.
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pubmed:affiliation |
Department of Cardiology and Pneumology, University Medicine Göttingen, Germany. jens.kockskaemper@meduni-graz.at
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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