| http://purl.uniprot.org/citations/22037186 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22037186 | http://www.w3.org/2000/01/rdf-schema#comment | "This study examines the extent to which the antiapoptotic Bcl-2 proteins Bcl-2 and Bcl-x(L) contribute to diabetic Ca(2+) dysregulation and vessel contractility in vascular smooth muscle cells (VSMCs) through their interaction with inositol 1,4,5-trisphosphate receptor (InsP(3)R) intracellular Ca(2+) release channels. Measurements of intracellular ([Ca(2+)](i)) and sarcoplasmic reticulum ([Ca(2+)](SR)) calcium concentrations were made in primary cells isolated from diabetic (db/db) and nondiabetic (db/m) mice. In addition, [Ca(2+)](i) and constriction were recorded simultaneously in isolated intact arteries. Protein expression levels of Bcl-x(L) but not Bcl-2 were elevated in VSMCs isolated from db/db compared with db/m age-matched controls. In single cells, InsP(3)-evoked [Ca(2+)](i) signaling was enhanced in VSMCs from db/db mice compared with db/m. This was attributed to alterations in the intrinsic properties of the InsP(3)R itself because there were no differences between db/db and db/m in the steady-state [Ca(2+)](SR) or InsP(3)R expression levels. Moreover, in permeabilized cells the rate of InsP(3)R-dependent SR Ca(2+) release was increased in db/db compared with db/m VSMCs. The enhanced InsP(3)-dependent SR Ca(2+) release was attenuated by the Bcl-2 protein inhibitor ABT-737 only in diabetic cells. Application of ABT-737 similarly attenuated enhanced agonist-induced [Ca(2+)](i) signaling only in intact aortic and mesenteric db/db vessels. In contrast, ABT-737 had no effect on agonist-evoked contractility in either db/db or db/m vessels. Taken together, the data suggest that in type 2 diabetes the mechanism for [Ca(2+)](i) dysregulation in VSMCs involves Bcl-2 protein-dependent increases in InsP(3)R excitability and that dysregulated [Ca(2+)](i) signaling does not appear to contribute to increased vessel reactivity."xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajpheart.00218.2011"xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/author | "White C."xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/author | "Velmurugan G.V."xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/name | "Am J Physiol Heart Circ Physiol"xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/pages | "H124-34"xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/title | "Calcium homeostasis in vascular smooth muscle cells is altered in type 2 diabetes by Bcl-2 protein modulation of InsP3R calcium release channels."xsd:string |
| http://purl.uniprot.org/citations/22037186 | http://purl.uniprot.org/core/volume | "302"xsd:string |
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