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J Appl Physiol (August 16, 2002). doi:10.1152/japplphysiol.00583.2002
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Articles in PresS, published online ahead of print August 16, 2002
J Appl Physiol, 10.1152/jap.00583.2002
Submitted on July 1, 2002
Accepted on August 14, 2002

Rescue of Contractile Abnormalities by Na+/Ca2+ Exchanger Overexpression in Post-Infarction Rat Myocytes

Xue-Qian Zhang1, Jianliang Song1, Anwer Qureshi2, Lawrence I Rothblum1, Lois L Carl1, Qiang Tian1, and Joseph Y Cheung2*

1 Weis Center for Research, Geisinger Medical Center, Danville, PA, USA
2 Weis Center for Research, Geisinger Medical Center, Danville, PA, USA; Department of Medicine, Geisinger Medical Center, Danville, PA, USA

* To whom correspondence should be addressed. E-mail: jcheung{at}geisinger.edu.

Previous studies on myocytes isolated from rat hearts 3 wks after myocardial infarction (MI) demonstrated increased cell length, reduced Na+/Ca2+ exchange (NCX1) activity, altered contractility and intracellular Ca2+ concentration ([Ca2+]i) transients. In the present study we investigated whether NCX1 overexpression in MI myocytes would restore contraction and [Ca2+]i transients to normal. When placed in culture under continued electrical field stimulation conditions, differences in contraction amplitudes and cell lengths between sham and MI myocytes were preserved for at least 48h. Infection of both sham and MI myocytes by adenovirus expressing green fluorescent protein (GFP) resulted in >95% infection as evidenced by GFP fluorescence, but contraction amplitudes at 6-, 24-, and 48-h post-infection were not affected. NCX1 overexpression in MI myocytes resulted in lower diastolic [Ca2+]i levels at all extracellular Ca2+ concentrations ([Ca2+]o) examined, suggesting enhanced forward Na+/Ca2+ exchange activity. At 5 mM [Ca2+]o, the subnormal contraction and [Ca2+]i transient amplitudes in MI myocytes (compared to sham myocytes) were restored towards normal levels by overexpressing NCX1. At 0.6 mM [Ca2+]o, the supranormal contraction and [Ca2+]i transient amplitudes in MI myocytes (compared to sham myocytes) were lowered by NCX1 overexpression. We conclude that overexpression of Na+/Ca2+ exchanger in MI myocytes was effective in improving contractile dysfunction, most likely due to enhancement of both Ca2+ efflux and influx during a cardiac cycle. We suggest that decreased Na+/Ca2+ exchange activity may play an important role in contractile abnormalities in postinfarction myocytes.




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