Source:http://linkedlifedata.com/resource/pubmed/id/16899570
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-8-10
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pubmed:abstractText |
Uterine artery endothelial cells (UAEC) derived from pregnant (P-UAEC) and nonpregnant (NP-UAEC) ewes retain pregnancy-specific differences in cell signaling as well as vasodilator production through passage 4. In particular, when P- and NP-UAEC are stimulated with ATP over a 2.5 min recording period, they exhibit similar initial transient peaks in the intracellular free Ca(2+) concentration ([Ca(2+)](i)), but the P-UAEC show a heightened sustained phase. In order to establish whether this was due to an altered subclass of purinergic receptor (P2), both the dose dependency of [Ca(2+)](i) responses to ADP and UTP and the profile of purinergic receptor expression are determined in NP- and P-UAEC. Our findings indicate that while several isoforms of P2X and P2Y receptors are present, it is P2Y2 that is responsible for the ATP-induced initial transient peak in both cell types. We also characterized several key components of the ATP-induced Ca(2+) signaling cascade, including the inositol 1,4,5-trisphosphate receptor and G-proteins, but could not confirm any pregnancy-specific variation in the protein expression that correlated with pregnancy-specific differences in prolonged Ca(2+) signaling. We thus investigated whether such a difference may be inherent to the cell itself rather than specific to the purinergic receptor-signaling pathway. Using thapsigargin (Tg), we were able to demonstrate that the initial Tg-sensitive intracellular pool of Ca(2+)is nearly identical with the capacity in both cell types, but the P-UAEC is nonetheless capable of greater capacitative Ca(2+) entry (CCE) than NP-UAEC. Furthermore, CCE induced by Tg could be dramatically inhibited by 2-aminoethoxydiphenyl borate, suggesting a role for store-operated channels in the ATP-induced [Ca(2+)](i) response. We conclude that changes at the level of capacitative entry mechanisms rather than switching of receptor subtype or coupling to phospholipase C underlies pregnancy adaptation of UAEC at the level of Ca(2+)signaling.
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pubmed:grant | |
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 |
Aug
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pubmed:issn |
0022-0795
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
190
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
373-84
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16899570-Adenosine Triphosphate,
pubmed-meshheading:16899570-Animals,
pubmed-meshheading:16899570-Arteries,
pubmed-meshheading:16899570-Blotting, Western,
pubmed-meshheading:16899570-Calcium,
pubmed-meshheading:16899570-Calcium Signaling,
pubmed-meshheading:16899570-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:16899570-Endothelial Cells,
pubmed-meshheading:16899570-Endothelium, Vascular,
pubmed-meshheading:16899570-Female,
pubmed-meshheading:16899570-GTP-Binding Proteins,
pubmed-meshheading:16899570-Microscopy, Fluorescence,
pubmed-meshheading:16899570-Models, Animal,
pubmed-meshheading:16899570-Pregnancy,
pubmed-meshheading:16899570-Receptors, Purinergic,
pubmed-meshheading:16899570-Sheep,
pubmed-meshheading:16899570-Uterus
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pubmed:year |
2006
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pubmed:articleTitle |
Pregnancy-enhanced Ca2+ responses to ATP in uterine artery endothelial cells is due to greater capacitative Ca2+ entry rather than altered receptor coupling.
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pubmed:affiliation |
Perinatal Research Laboratories, Department of Obstetrics and Gynecology, University of Wisconsin - Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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