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J. Biol. Chem., Vol. 281, Issue 44, 33477-33486, November 3, 2006

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Azumolene Inhibits a Component of Store-operated Calcium Entry Coupled to the Skeletal Muscle Ryanodine Receptor^*

Xiaoli Zhao, Noah Weisleder, Xuehai Han, Zui Pan, Jerome Parness, Marco Brotto¹, and Jianjie Ma

From the Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Piscataway, New Jersey 08854 and the Department of Anesthesiology, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213

Dantrolene reduces the elevated myoplasmic Ca²⁺ generated during malignant hyperthermia, a pharmacogenetic crisis triggered by volatile anesthetics. Although specific binding of dantrolene to the type 1 ryanodine receptor (RyR1), the Ca²⁺ release channel of skeletal muscle sarcoplasmic reticulum, has been demonstrated, there is little evidence for direct dantrolene inhibition of RyR1 channel function. Recent studies suggest store-operated Ca²⁺ entry (SOCE) contributes to skeletal muscle function, but the effect of dantrolene on this pathway has not been examined. Here we show that azumolene, an equipotent dantrolene analog, inhibits a component of SOCE coupled to activation of RyR1 by caffeine and ryanodine, whereas the SOCE component induced by thapsigargin is not affected. Our data suggest that azumolene distinguishes between two mechanisms of cellular signaling to SOCE in skeletal muscle, one that is coupled to and one independent from RyR1.

Received for publication, March 10, 2006 , and in revised form, August 29, 2006.

^* This work was supported by National Institutes of Health Grants RO1-AG15556, RO1-HL69000, RO1-CA95739 (to J. M.), and RO1-AR45593 (to J. P.), an NIA Faculty Development grant from the National Institutes of Health, American Heart Association Scientist Development Grant 0530132N (to M. B.), and an American Heart Association postdoctoral fellowship (to N. W.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, 683 Hoes Lane, Piscataway, NJ 08854. Tel.: 732-235-5068; Fax: 732-235-4483; E-mail: brottoma{at}umdnj.edu.

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