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J. Biol. Chem., Vol. 279, Issue 20, 21287-21293, May 14, 2004

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Decreased Expression of Ryanodine Receptors Alters Calcium-induced Calcium Release Mechanism in mdx Duodenal Myocytes^*

Jean-Luc Morel, Lala Rakotoarisoa, Loice H. Jeyakumar, Sidney Fleischer, Chantal Mironneau, and Jean Mironneau

From the Laboratoire de Signalisation et Interactions Cellulaires, CNRS UMR 5017, Université de Bordeaux II, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France and the Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee 37235

It is generally believed that alterations of calcium homeostasis play a key role in skeletal muscle atrophy and degeneration observed in Duchenne's muscular dystrophy and mdx mice. Mechanical activity is also impaired in gastrointestinal muscles, but the cellular and molecular mechanisms of this pathological state have not yet been investigated. We showed, in mdx duodenal myocytes, that both caffeine- and depolarization-induced calcium responses were inhibited, whereas acetylcholine- and thapsigargin-induced calcium responses were not significantly affected compared with control mice. Calcium-induced calcium release efficiency was impaired in mdx duodenal myocytes depending only on inhibition of ryanodine receptor expression. Duodenal myocytes expressed both type 2 and type 3 ryanodine receptors and were unable to produce calcium sparks. In control and mdx duodenal myocytes, both caffeine- and depolarization-induced calcium responses were dose-dependently and specifically inhibited with the anti-type 2 ryanodine receptor antibody. A strong inhibition of type 2 ryanodine receptor in mdx duodenal myocytes was observed on the mRNA as well as on the protein level. Taken together, our results suggest that inhibition of type 2 ryanodine receptor expression in mdx duodenal myocytes may account for the decreased calcium release from the sarcoplasmic reticulum and reduced mechanical activity.

Received for publication, October 9, 2003 , and in revised form, February 3, 2004.

^* This work was supported by a grant from the Association Française contre les Myopathies (France). 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.

To whom correspondence should be addressed. Tel.: 33-5-57-57-12-31; Fax: 33-5-57-57-12-27; E-mail: jean.mironneau{at}umr5017.u-bordeaux2.fr.

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