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Calcium signaling in mast cells: focusing on L-type calcium channels.

Authors
  • Suzuki, Yoshihiro1
  • Inoue, Toshio
  • Ra, Chisei
  • 1 Division of Molecular Cell Immunology and Allergology, Nihon University Graduate School of Medical Science, 30-1 Oyaguchikami-cho Itabashi-ku, Tokyo 173-8610, Japan. [email protected] , (Japan)
Type
Published Article
Journal
Advances in experimental medicine and biology
Publication Date
Jan 01, 2012
Volume
740
Pages
955–977
Identifiers
DOI: 10.1007/978-94-007-2888-2_44
PMID: 22453979
Source
Medline
License
Unknown

Abstract

Mast cells play central roles in adaptive and innate immunity. IgE-dependent stimulation of the high-affinity IgE receptor (FcεRI) results in rapid secretion of various proinflammatory chemical mediators and cytokines. All of the outputs depend to certain degrees on an increase in the intracellular Ca(2+) concentration, and influx of Ca(2+) from the extracellular space is often required for their full activation. There is strong evidence that FcεRI stimulation induces two different modes of Ca(2+) influx, store-operated Ca(2+) entry (SOCE) and non-SOCE, which are activated in response to endoplasmic reticulum Ca(2+) store depletion and independently of Ca(2+) store depletion, respectively, in mast cells. Although Ca(2+) release-activated Ca(2+) channels are the major route of SOCE, recent evidence indicates that they are not the only Ca(2+) channels activated by Ca(2+) store depletion. The recent data suggest that L-type Ca(2+) channels, which were thought to be a characteristic feature of excitable cells, exist in mast cells to mediate non-SOCE, which is critical for protecting mast cells against activation-induced mitochondrial cell death. In this chapter, we provide an overview of recent advances in our understanding of Ca(2+) signaling in mast cells with a special attention to the emerging role for the L-type Ca(2+) channels as a regulator of mast cell survival.

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