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Biological Research

Print version ISSN 0716-9760

Biol. Res. vol.37 no.4 Santiago  2004 



Biol Res 37: 495, 2004



Cytosolic free calcium concentration is a key regulatory factor and perhaps the most widely used means of controlling cellular function. Increases in intracellular free calcium concentration in response to extracellular signals can initiate and modulate many different cellular events, which include short-term responses such as muscle contraction and secretion as well as long-term responses including cell growth and proliferation and the expression of genes required for memory and learning. Furthermore, an alteration of intracellular calcium homeostasis is an early event in apoptosis and in the development of irreversible cell injury and necrosis.

Calcium can enter cells through different pathways, which are activated by specific stimuli including membrane depolarization, chemical signals and calcium depletion of intracellular stores. Calcium can also be released from intracellular stores through inositol 1,4,5-trisphosphate (InsP3) receptor channels (InsP3R channels) or Ryanodine receptor channels (RyR channels). Recent findings indicate that cells also possess nicotinic acid adenine dinucleotide phosphate (NAADP)-sensitive calcium stores and that mitochondria have an important role in the generation of specific calcium signals. The calcium signals generated by these diverse mechanisms are highly organized in space, frequency, and amplitude, and it is becoming increasingly apparent that changes of free calcium concentration with time as well as their spatial localization convey specific information to cells.

Research in the field of calcium release and cellular calcium signals has emerged in recent years as one of the central themes in modern cell biology and cell physiology. It has been established that a given stimulus can either activate primarily one specific calcium-signaling pathway or trigger a series of different pathways. Therefore, the final cellular response is the result of the integration of all the different calcium signaling pathways implicated. The ensuing behavior of the cell is manifested either by rapid transient responses or by slower responses that entail more permanent changes at the gene expression level.

Accordingly, it becomes highly relevant and timely to analyze in an integrated context the different players that give rise to calcium signals mediated by different calcium release channels. This was the central aim of the international workshop on "Calcium release and cellular calcium signaling domains" held last year in Marbella, Chile (all speaker and poster abstracts were published in a preceding issue of Biological Research). This workshop, which corresponds to the second annual international meeting organized by the FONDAP Center for Molecular Studies of the Cell, congregated many speakers who have made seminal contributions to world science in the field of calcium signaling. It is worthy of note that many speakers had not met before, although by working on the different aspects of calcium signaling, they certainly knew their respective publications. Special emphasis was placed on inviting younger and emerging scientists along with more established investigators, as well as students who primarily came from Latin American countries. On behalf of the local calcium-signaling group I wish to thank everyone involved for making this superb workshop possible in Chile. Judging from the many comments received after the workshop, the groundbreaking conjunction of these researchers at the workshop proved very fruitful. It certainly contributed to a particularly exciting and highly stimulating atmosphere that we hope was greatly valuable to all the participants.

Nearly all of the speakers at the workshop agreed to write short reviews on the subjects of their talks. We trust these articles will benefit the community of researchers worldwide who work on the many aspects of the calcium-signaling field. We also genuinely believe that in addition to advancing basic knowledge, the extensive discussion of the mechanism involved in normal calcium signaling should provide some understanding of abnormal calcium signaling processes that are altered in diseased individuals.



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