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Articles in PresS, published online ahead of print May 2, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00197.2002
Submitted on March 6, 2002
Accepted on April 12, 2002
1 Weis Center for Research, Geisinger Medical Center, Danville, Pennsylvania, USA
2 Weis Center for Research, Geisinger Medical Center, Danville, Pennsylvania, USA; Medicine, Geisinger Medical Center, Danville, Pennsylvania, USA
* To whom correspondence should be addressed. E-mail: jcheung{at}geisinger.edu.
Previous studies have shown that phospholemman (PLM) expression was increased after myocardial infarction (MI) in rats (Sehl PD et al., Circulation 101:1990-1999, 2000). The present study was undertaken to test the hypothesis that, in normal adult rat cardiac myocytes, PLM overexpression alters contractile function and and [Ca2+]i homeostasis in a manner similar to that observed in post-MI myocytes. Compared to myocytes infected by control adenovirus expressing green fluorescent protein (GFP) alone, Western blots indicated a 41% increase in PLM expression after 72h (p<0.001) but no changes in the levels of Na+/Ca2+ exchanger, sarcoplasmic reticulum Ca2+-ATPase and calsequestrin levels in myocytes infected by adenovirus expressing both GFP and PLM. At extracellular Ca2+ concentration ([Ca2+]o) of 5 mM, maximal contraction amplitudes in PLM-overexpressed myocytes were 24% (p<0.005) and [Ca2+]i transient amplitudes were 18% (p<0.05) lower than control myocytes. At 0.6 mM [Ca2+]o, however, contraction and [Ca2+]i transient amplitudes were significantly (p<0.05) higher in PLM- overexpressed than control myocytes by 18% and 42%, respectively. This pattern of contractile and [Ca2+]i transient abnormalities in PLM overexpressed myocytes mimics that observed in post-MI rat myocytes (Zhang XQ et al., J. Appl. Physiol. 86:943-950, 1999). We suggest that PLM overexpression observed in post-MI myocytes may partly account for the contractile abnormalities by perturbing Ca2+ fluxes during excitation-contraction.
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