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J. Biol. Chem., Vol. 278, Issue 37, 35168-35171, September 12, 2003

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Involvement of Protein Kinase C- in Inositol Hexakisphosphate-induced Exocytosis in Mouse Pancreatic -Cells^*

Marianne Høy  , Per-Olof Berggren ¶ and Jesper Gromada  ||

From the Laboratory of Islet Cell Physiology, Novo Nordisk A/S, Novo Alle, DK-2880 Bagsvaerd, Denmark and ^¶The Rolf Luft Center for Diabetes Research, Department of Molecular Medicine, Karolinska Institutet, S-171 76 Stockholm, Sweden

Inositolhexakisphosphate (InsP₆) plays a pivotal role in the pancreatic -cell stimulus-secretion coupling. We have used capacitance measurements to study the effects of InsP₆ on Ca²⁺-dependent exocytosis in single mouse pancreatic -cells. In the presence of inhibitors of the protein phosphatase calcineurin to block endocytosis, intracellular application of InsP₆ produced a dose-dependent stimulation of exocytosis, and half-maximal effect was observed at 22 µM. The stimulatory effect of InsP₆ was dependent on protein kinase C (PKC) activity. Antisense oligonucleotides directed against specific PKC isoforms (, II, , , ) revealed the involvement of PKC- in InsP₆-induced exocytosis. Furthermore, expression of dominant negative PKC- abolished InsP₆-evoked exocytosis, whereas expression of wild-type PKC- led to a significant stimulation of InsP₆-induced exocytosis. These data demonstrate that PKC- is involved in InsP₆-induced exocytosis in pancreatic -cells.

Received for publication, April 15, 2003 , and in revised form, June 26, 2003.

^* This study was supported in part by the National Institutes of Health (Grant DK 58508), the Swedish Research Council, the Swedish Diabetes Association, the Novo Nordisk Foundation, the Juvenile Diabetes Foundation International, and the Funds of Karolinska Institutet. 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.

A recipient of a scholarship from the Academy of Technical Sciences and Novo Nordisk A/S. Present address: Dept. of Medical Physiology, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark.

^|| To whom correspondence may be addressed: Lilly Research Laboratories, Essener Strasse 93, D-22419 Hamburg, Germany. Tel.: 49-40-527-24-323; Fax: 49-40-527-24-615; E-mail: gromada{at}lilly.com.

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