Abstract：
:Ca(2+) is known as a universal messenger mediating a wide variety of cellular processes, including cell death. In fact, this ion has been proposed as the 'cell death master', not only at the intracellular but also at the intercellular level. The most direct form of intercellular spread of cell death is mediated by gap junction channels. These channels have been shown to propagate cell death as well as cell survival signals between the cytoplasm of neighbouring cells, reflecting the dual role of Ca(2+) signals, i.e. cell death versus survival. Its precursor, the unopposed hemichannel (half of a gap junction channel), has recently joined in as a toxic pore connecting the intracellular with the extracellular environment and allowing the passage of a range of substances. The biochemical nature of the so-called intercellular cell death molecule, transferred through gap junctions or released/taken up via hemichannels, remains elusive but several studies pinpoint Ca(2+) itself or its messenger inositol trisphosphate as the responsible masters in crime. Although direct evidence is still lacking, indirect data including Ca(2+) involvement in intercellular communication and cell death, and effects of intercellular communication on intracellular Ca(2+) homeostasis, support this hypothesis. In addition, hemichannels and their molecular building blocks, connexin or pannexin proteins, may exert their effects on Ca(2+)-dependent cell death at the intracellular level, independently from their channel functions. This review provides a cutting edge overview of the current knowledge and underscores the intimate connection between intercellular communication, Ca(2+) signalling and cell death.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Decrock E,Vinken M,Bol M,D'Herde K,Rogiers V,Vandenabeele P,Krysko DV,Bultynck G,Leybaert Ldoi
10.1016/j.ceca.2011.05.007subject
Has Abstractpub_date
2011-09-01 00:00:00pages
310-21issue
3eissn
0143-4160issn
1532-1991pii
S0143-4160(11)00092-3journal_volume
50pub_type
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