PMID:11919174

Citation	Song, G, Harding, SE, Duchen, MR, Tunwell, R, O'Gara, P, Hawkins, TE and Moss, SE (2002) Altered mechanical properties and intracellular calcium signaling in cardiomyocytes from annexin 6 null-mutant mice. FASEB J. 16:622-4
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.
Links	PubMed
Keywords	Animals; Annexin A6/genetics; Annexin A6/physiology; Biomechanics; Caffeine/pharmacology; Calcium Signaling; Cells, Cultured; Cytoplasm/metabolism; Gene Targeting; Kinetics; Mice; Mice, Knockout; Models, Cardiovascular; Myocardial Contraction; Myocardium/metabolism
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