Linked Life Data

16249429

Source:http://linkedlifedata.com/resource/pubmed/id/16249429

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pubmed-article:16249429pubmed:abstractTextThe defects identified in the mechanical activity of the hearts from type 1 diabetic animals include alteration of Ca2+ signaling via changes in critical processes that regulate intracellular Ca2+ concentration. These defects result partially from a dysfunction of cardiac ryanodine receptor calcium release channel (RyR2). The present study was designed to determine whether the properties of the Ca2+ sparks might provide insight into the role of RyR2 in the altered Ca2+ signaling in cardiomyocytes from diabetic animals when they were analyzed together with Ca2+ transients. Basal Ca2+ level as well as Ca2+-spark frequency of cardiomyoctes isolated from 5-week streptozotocin (STZ)-induced diabetic rats significantly increased with respect to aged-matched control rats. Ca2+ transients exhibited significantly reduced amplitude and prolonged time courses as well as depressed Ca2+ loading of sarcoplasmic reticulum in diabetic rats. Spatio-temporal properties of the Ca2+ sparks in cardiomyocytes isolated from diabetic rats were also significantly altered to being almost parallel to the changes of Ca2+ transients. In addition, RyR2 from diabetic rat hearts were hyperphosphorylated and protein levels of both RyR2 and FKBP12.6 depleted. These data show that STZ-induced diabetic rat hearts exhibit altered local Ca2+ signaling with increased basal Ca2+ level.lld:pubmed
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pubmed-article:16249429pubmed:articleTitleEffects of diabetes on ryanodine receptor Ca release channel (RyR2) and Ca2+ homeostasis in rat heart.lld:pubmed
pubmed-article:16249429pubmed:affiliationDepartment of Biophysics, School of Medicine, Ankara University, Ankara, Turkey.lld:pubmed
pubmed-article:16249429pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16249429pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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