AIMS: Plasmalemmal Ca(2+)-ATPase (PMCA) is involved in Ca(2+) handling and the regulation of intracellular signalling pathways in the heart. However, there is no information on its functioning in heart hypertrophy and failure. We aimed to investigate the Ca(2+)-transporting ability of PMCA, Na(+)/Ca(2+) exchanger (NCX), and sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA2a), as well as the amplitude of Ca(2+) transients and cell shortening in myocytes isolated from rat hearts at various time intervals after myocardial infarction (MI). METHODS AND RESULTS: The rate of Ca(2+) transport by PMCA, NCX, and SERCA2a was estimated from the rate constants of decay of electrically and caffeine-evoked Ca(2+) transients in left ventricular myocytes isolated 1 week, 1 month, and 3 months after MI. One week, 1 month, and 3 months after MI, the transporting function of PMCA decreased by 27, 41, and 67%, respectively, compared with that in time-matched sham animals. This was accompanied by increased amplitude of Ca(2+) transients, cell shortening, and SR Ca(2+) content. Carboxyeosin, a blocker of PMCA, increased the amplitude of shortening in cells extracted from control hearts. This effect was absent 1 and 3 months after MI. PMCA1, 2, and 4 mRNAs were unchanged in the ventricular muscle 3 months after MI when compared with time-matched sham animals. The transporting function of NCX was increased by 65% only 3 months after MI, whereas that of SERCA2a was decreased by approximately 18% at all three time points after MI. CONCLUSION: The ability of PMCA to transport Ca(2+) progressively decreases over 3 months after MI. This decrease may contribute to the increase in amplitude of Ca(2+) transients and myocyte shortening.
AIMS: Plasmalemmal Ca(2+)-ATPase (PMCA) is involved in Ca(2+) handling and the regulation of intracellular signalling pathways in the heart. However, there is no information on its functioning in heart hypertrophy and failure. We aimed to investigate the Ca(2+)-transporting ability of PMCA, Na(+)/Ca(2+) exchanger (NCX), and sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA2a), as well as the amplitude of Ca(2+) transients and cell shortening in myocytes isolated from rat hearts at various time intervals after myocardial infarction (MI). METHODS AND RESULTS: The rate of Ca(2+) transport by PMCA, NCX, and SERCA2a was estimated from the rate constants of decay of electrically and caffeine-evoked Ca(2+) transients in left ventricular myocytes isolated 1 week, 1 month, and 3 months after MI. One week, 1 month, and 3 months after MI, the transporting function of PMCA decreased by 27, 41, and 67%, respectively, compared with that in time-matched sham animals. This was accompanied by increased amplitude of Ca(2+) transients, cell shortening, and SR Ca(2+) content. Carboxyeosin, a blocker of PMCA, increased the amplitude of shortening in cells extracted from control hearts. This effect was absent 1 and 3 months after MI. PMCA1, 2, and 4 mRNAs were unchanged in the ventricular muscle 3 months after MI when compared with time-matched sham animals. The transporting function of NCX was increased by 65% only 3 months after MI, whereas that of SERCA2a was decreased by approximately 18% at all three time points after MI. CONCLUSION: The ability of PMCA to transport Ca(2+) progressively decreases over 3 months after MI. This decrease may contribute to the increase in amplitude of Ca(2+) transients and myocyte shortening.
Authors: Francisco Altamirano; José M Eltit; Gaëlle Robin; Nancy Linares; Xudong Ding; Isaac N Pessah; Paul D Allen; José R López Journal: J Biol Chem Date: 2014-05-20 Impact factor: 5.157
Authors: David E Lanfear; Jasmine A Luzum; Ruicong She; Hongsheng Gui; Mark P Donahue; Christopher M O'Connor; Kirkwood F Adams; Sandra Sanders-van Wijk; Nicole Zeld; Micha T Maeder; Hani N Sabbah; William E Kraus; Hans-Peter Brunner-LaRocca; Jia Li; L Keoki Williams Journal: Circ Heart Fail Date: 2020-10-04 Impact factor: 8.790