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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:
  • Authors:
    Song G, Harding SE, Duchen MR, Tunwell R, O'Gara P, Hawkins TE, Moss SE
  • Publication date:
  • Pagination:
    622, 624
  • Journal:
    The FASEB Journal
  • Volume:
  • Issue:
  • Print ISSN:
  • 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
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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