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Effects of Diabetes on Ryanodine Receptor Ca Release Channel (RyR2) and Ca²⁺ Homeostasis in Rat Heart

¹ Department of Biophysics, School of Medicine, Ankara University, Ankara, Turkey
² Department of Pharmacology, School of Medicine, Ankara University, Ankara, Turkey
³ Department of Biophysics, School of Medicine, Hacettepe University, Ankara, Turkey
⁴ INSERM U-637, Physiopathologie Cardiovasculaire, CHU Arnaud de Villeneuve, Montpellier, France

The 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.

Abbreviations: RyR2, ryanodine receptor Ca release channel; SR, sarcoplasmic reticulum; STZ, streptozotocin

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