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Volume 272, Number 10, Issue of March 7, 1997 pp. 6699-6705
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

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Opioid Peptide Gene Expression in the Primary Hereditary Cardiomyopathy of the Syrian Hamster
III. AUTOCRINE STIMULATION OF PRODYNORPHIN GENE EXPRESSION BY DYNORPHIN B

(Received for publication, July 15, 1996, and in revised form, November 18, 1996)

Carlo Ventura ^§ and Gianfranco Pintus ^§

From the  Institute of Biological Chemistry "A. Bonsignore," School of Medicine, University of Sassari, Viale San Pietro 43/B, 07100 Sassari, Italy, and the ^§ National Laboratory of the National Institute of Biostructures and Biosystems, Osilo, Italy

Prodynorphin mRNA and dynorphin B expression have been previously shown to be greatly increased in cardiac myocytes of BIO 14.6 cardiomyopathic hamsters. Here we report that exogenous dynorphin B induced a dose-dependent increase in prodynorphin mRNA levels and stimulated prodynorphin gene transcription in normal hamster myocytes. Similar responses were elicited by the synthetic selective  opioid receptor agonist U-50,488H. These effects were counteracted by the  opioid receptor antagonist Mr-1452 and were not observed in the presence of chelerythrine or calphostin C, two specific protein kinase C (PKC) inhibitors. Treatment of cardiomyopathic cells with Mr-1452 significantly decreased both prodynorphin mRNA levels and prodynorphin gene transcription. In control myocytes, dynorphin B induced the translocation of PKC- to the nucleus and increased nuclear PKC activity without affecting the expression of PKC-, -, or -. Acute release of either U-50,488H or dyn B over single normal or cardiomyopathic cells transiently increased the cytosolic Ca²⁺ concentration. A sustained treatment with each opioid agonist increased the cytosolic Ca²⁺ level for a more prolonged period in cardiomyopathic than in control myocytes and led to a depletion of Ca²⁺ from the sarcoplasmic reticulum in both groups of cells. The possibility that prodynorphin gene expression may affect the function of the cardiomyopathic cell through an autocrine mechanism is discussed.

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