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Publication Detail
Calcium microdomains and oxidative stress.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Davidson SM, Duchen MR
  • Publication date:
    11/2006
  • Pagination:
    561, 574
  • Journal:
    Cell Calcium
  • Volume:
    40
  • Issue:
    5
  • Print ISSN:
    0143-4160
  • Keywords:
    Animals, Calcium, Calcium Signaling, Inositol 1, 4, 5-Trisphosphate Receptors, Membrane Microdomains, metabolism, Mitochondria, Mitochondrial Membrane Transport Proteins, Myocytes, Cardiac, Oxidation-Reduction, Oxidative Stress, physiology, Reactive Oxygen Species, Ryanodine Receptor Calcium Release Channel, Sarcoplasmic Reticulum Calcium-Transporting ATPases
  • Addresses:
    The Hatter Cardiovascular Institute, Royal Free and University College Medical School, London, Department of Medicine, 67 Chenies Mews, London, UK. s.davidson@ucl.ac.uk
  • Notes:
    Imported from PubMed 14/04/2008, 74 DA - 20061107IS - 0143-4160 (Print)LA - engPT - Journal ArticleRN - 0 (Inositol 1,4,5-Trisphosphate Receptors)RN - 0 (Mitochondrial Membrane Transport Proteins)RN - 0 (Reactive Oxygen Species)RN - 0 (Ryanodine Receptor Calcium Release Channel)RN - 0 (mitochondrial permeability transition pore)RN - 7440-70-2 (Calcium)RN - EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)SB - IM
Abstract
The phenomenon of calcium microdomains is firmly established in the field of subcellular physiology. These regions of localized, transient calcium increase are exemplified by the spontaneous 'sparks' released through the ryanodine receptor in myocytes, but include subplasmalemmal microdomains, focal calcium oscillations and microdomains enclosed within organelles, such as the endoplasmic reticulum, golgi and mitochondria. Increasing evidence suggests that oxidative stress regulates both the formation and disappearance of microdomains. Calcium release channels and transporters are all modulated by redox state, while several mechanisms that generate oxidative or nitrosative stress are regulated by calcium. Here, we discuss the evidence for the regulation of calcium microdomains by redox state, and, by way of example, demonstrate that the frequency of calcium sparks in cardiomyocytes is increased in response to oxidative stress. We consider the evidence for the existence of analogous microdomains of reactive oxygen and nitrogen species and suggest that the refinement of imaging techniques for these species might lead to similar concepts. The interaction between Ca(2+) microdomains and proteins that modulate their formation results in a complex and dynamic, spatial signaling mechanism, which is likely to be broadly applicable to different cell types, adding new dimensions to the calcium signaling 'toolkit'
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