Larry R. Jones

School of Medicine, Medicine, Cardiology

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Overexpression of junctin causes adaptive changes in cardiac myocyte Ca²⁺ signaling

Uwe Kirchhefer; Gabriela Hanske; Larry R. Jones; Isabel Justus; Lars Kaestner; Peter Lipp; Wilhelm Schmitz; Joachim Neumann (Profiled Author: Larry R. Jones)

Cell Calcium. 2006;39(2):131-142.

In cardiac muscle, junctin forms a quaternary protein complex with the ryanodine receptor (RyR), calsequestrin, and triadin 1 at the luminal face of the junctional sarcoplasmic reticulum (jSR). By binding directly the RyR and calsequestrin, junctin may mediate the Ca²⁺ -dependent regulatory interactions between both proteins. To gain more insight into the underlying mechanisms of impaired contractile relaxation in transgenic mice with cardiac-specific overexpression of junctin (TG), we studied cellular Ca²⁺ handling in these mice. We found that the SR Ca²⁺ load was reduced by 22% in cardiomyocytes from TG mice. Consistent with this, the frequency of Ca²⁺ sparks was diminished by 32%. The decay of spontaneous Ca²⁺ sparks was prolonged by 117% in TG. This finding was associated with a lower Na⁺-Ca²⁺ exchanger (NCX) protein expression (by 67%) and a higher basal RyR phosphorylation at Ser²⁸⁰⁹ (by 64%) in TG. The shortening- and Δ[Ca]i-frequency relationships (0.5-4 Hz) were flat in TG compared to wild-type (WT) which exhibited a positive staircase for both parameters. Furthermore, increasing stimulation frequencies hastened the time of relaxation and the decay of [Ca]i by a higher percentage in TG. We conclude that the impaired relaxation in TG may result from a reduced NCX expression and/or a higher SR Ca²⁺ leak. The altered shortening-frequency relationship in TG seems to be a consequence of an impaired excitation-contraction coupling with depressed SR Ca²⁺ release at higher rates of stimulation. Our data suggest that the more prominent frequency-dependent hastening of relaxation in TG results from a stimulation of SR Ca²⁺ transport reflected by corresponding changes of [Ca]i. © 2005 Elsevier Ltd. All rights reserved.

PMID: 16289269    

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