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Published online 19 April 2004. doi:10.1083/jcb.200311061
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 2, 223-232
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Article

 Long-term modulation of mitochondrial Ca2+ signals by protein kinase C isozymes

Paolo Pinton1, Sara Leo1, Mariusz R. Wieckowski1, Giulietta Di Benedetto2, and Rosario Rizzuto1

1 Section of General Pathology, Department of Experimental and Diagnostic Medicine, Telethon Center for Cell Imaging and Interdisciplinary Center for the Study of Inflammation, University of Ferrara, 44100 Ferrara, Italy
2 Venetian Institute of Molecular Medicine, 35129 Padova, Italy

Address correspondence to R. Rizzuto, Section of General Pathology, Department of Experimental and Diagnostic Medicine, Via Borsari 46, 44100 Ferrara, Italy. Tel.: 39 0532 291361. Fax: 39 0532 247278. email: r.rizzuto{at}unife.it

The modulation of Ca2+ signaling patterns during repetitive stimulations represents an important mechanism for integrating through time the inputs received by a cell. By either overexpressing the isoforms of protein kinase C (PKC) or inhibiting them with specific blockers, we investigated the role of this family of proteins in regulating the dynamic interplay of the intracellular Ca2+ pools. The effects of the different isoforms spanned from the reduction of ER Ca2+ release (PKC{alpha}) to the increase or reduction of mitochondrial Ca2+ uptake (PKC{zeta} and PKCß/PKC{delta}, respectively). This PKC-dependent regulatory mechanism underlies the process of mitochondrial Ca2+ desensitization, which in turn modulates cellular responses (e.g., insulin secretion). These results demonstrate that organelle Ca2+ homeostasis (and in particular mitochondrial processing of Ca2+ signals) is tuned through the wide molecular repertoire of intracellular Ca2+ transducers.

Key Words: organelle; aequorin; calcium; kinases; signal transduction

Abbreviations used in this paper: {Delta}{Psi}m, mitochondrial membrane potential; AEQ, aequorin; IP3, inositol 1,4,5 trisphosphate; ROS, reactive oxygen species.


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