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Publication Detail
Altered mechanical properties and intracellular calcium signaling in cardiomyocytes from annexin 6 null-mutant mice
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Song G, Harding SE, Duchen MR, Tunwell R, O'Gara P, Hawkins TE, Moss SE
  • Publication date:
    2002
  • Pagination:
    622, 624
  • Journal:
    The FASEB Journal
  • Volume:
    16
  • Issue:
    6
  • Print ISSN:
    0892-6638
  • Keywords:
    ACT, amplitude, Animal, annexin, Annexin VI, As, Biomechanics, Ca2+, caffeine, calcium, calcium channel, Calcium Signaling, CALCIUM-BINDING PROTEIN, Calcium-Binding Proteins, cardiac, cardiomyocyte, cardiomyocytes, Cells, Cultured, channel, contractility, control, Cytoplasm, decay, Disruption, FAILURE, families, family, GENE, Gene Targeting, genetics, heart, heart failure, HEART-FAILURE, IM, in vitro, In-vitro, INCREASE, INTACT, Kinetics, knockout, LA, LIGHT, mammalian, mechanical, Mechanical properties, MECHANICAL-PROPERTIES, MECHANICS, metabolism, mice, Mice, Knockout, Models, Cardiovascular, modulator, mouse, Myocardial Contraction, Myocardium, myocytes, ophthalmology, pharmacology, physiology, Properties, Property, PROTEIN, Proteins, PUBLISHED, RATES, regulation, Removal, Result, TARGETED DISRUPTION, Tissue, Tissues, Universities, VITRO, heart failure, homeostasis, knockout, stimulus response coupling
Abstract
Annexin 6 is one of a widely expressed family of calcium-binding proteins found in most mammalian tissues, including the heart. Several studies have implicated annexin 6 in the regulation of intracellular Ca2+ signaling, and it has been shown in vitro to act as a modulator of the sarcoplasmic reticulum Ca2+-release channel, cardiac L-type calcium channel, and Na+/Ca2+ exchanger. To investigate the role of annexin 6 in intact cardiomyocytes, we used mice containing a targeted disruption of the annexin 6 gene. Compared with controls, the myocytes of annexin 6 null-mutant mice demonstrated a significant increase in the rates of shortening and relengthening. Intracellular Ca2+ transients in fura-2-loaded cardiomyocytes induced by caffeine showed a normal baseline and amplitude, whereas the rate of decay was doubled in annexin 6-/- myocytes compared with control mice. These results show that annexin 6 knockout in the mouse leads to an increase in myocyte contractility and faster diastolic Ca2+ removal from the cytoplasm. In light of published findings showing annexin 6 to be down-regulated in end-stage heart failure, these results are consistent with a role for annexin 6 as a negative inotropic factor in the regulation of cardiomyocyte mechanics
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