NDLI: Depletion of $Ca^{2+}$ from the sarcoplasmic reticulum of cardiac muscle prompts phosphorylation of phospholamban to stimulate store refilling

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Depletion of $Ca^{2+}$ from the sarcoplasmic reticulum of cardiac muscle prompts phosphorylation of phospholamban to stimulate store refilling

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Depletion of $Ca^{2+}$ from the sarcoplasmic reticulum of cardiac muscle prompts phosphorylation of phospholamban to stimulate store refilling

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bhogal, M. S. Colyer, J.
Description	Author Affiliation: Bhogal MS ( School of Biochemistry and Molecular Biology, University of Leeds, Leeds, LS2 9JT United Kingdom.);
Abstract	Nonmuscle cells have almost ubiquitously evolved a mechanism to detect and prevent Ca2+ store depletion-store operated calcium entry. No such mechanism has, as yet, been reported in cardiac myocytes. However, it is conceivable that such a mechanism may play an important role in cardiac Ca2+ homeostasis to ensure the availability of sufficient stored Ca2+ to maintain normal excitation contraction coupling. We present data that confirms the presence of a mechanism that is able to monitor the Ca2+ load of the SR and initiate a signaling process to accelerate Ca2+ uptake by the SR when store depletion is detected. Depletion of SR Ca2+ activates a protein kinase, the principal SR substrate of which is phospholamban. Phosphorylation of this SR protein promotes Ca2+ pump activity and therefore store refilling. Furthermore, a protein kinase activity associated with the SR that is inhibited by Ca2+ ions has been identified. We have measured lumenal [Ca2+] by using a fluorescent Ca2+ indicator and found that by initiating Ca2+ uptake and increasing Ca2+ load, we can inhibit the protein kinase activity associated with the SR. This confirms that a protein kinase, that is regulated by lumenal [Ca2+], has been identified and represents part of a previously unidentified signalling cascade. This local feedback mechanism would allow the myocyte to detect and prevent SR Ca2+ load depletion.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	4
Volume Number	95
Language	English
Publisher	National Academy of Sciences
Publisher Date	1998-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcium-Binding Proteins Metabolism Calcium Myocardium Sarcoplasmic Reticulum Animals Biological Transport, Active Calcium-Transporting ATPases Antagonists & Inhibitors Cell Compartmentation Cyclic AMP-Dependent Protein Kinases Enzyme Inhibitors Pharmacology Fluorescent Dyes Phosphorylation Phosphoserine Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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