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Am J Physiol Cell Physiol (November 21, 2001). doi:10.1152/ajpcell.00494.2001
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Articles in PresS, published online ahead of print November 20, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00494.2001
Submitted on October 16, 2001
Accepted on November 19, 2001

ENHANCEMENT OF L-TYPE CALCIUM CURRENT FROM NEONATAL MOUSE VENTRICULAR MYOCYTES BY PROTEIN KINASE C-ßII

Kris J Alden1, Paul H Goldspink2, Stuart W Ruch2, Peter M Buttrick2, and Jesus Garcia1*

1 Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL, USA
2 Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, IL, USA

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

The cardiac L-type calcium current (ICa) can be modified by activation of protein kinase C (PKC). However, the effect of PKC activation on ICa is still controversial. While some studies have shown a decrease in current, other studies report a biphasic effect (increase followed by decrease of current or viceversa). A possible explanation for the conflicting results is that several isoforms of PKC with opposing effects on the ICa were activated simultaneously. Here we examined the influence of a single PKC isoform (PKC-ßII) on L-type calcium channels in isolation from other cardiac isoforms using a transgenic mouse that conditionally expresses PKC-ßII. Ventricular cardiac myocytes were isolated from newborn mice and examined for expression of the transgene using single cell RT-PCR after ICa recording. Cells expressing PKC-ßII showed a 2-fold increase in nifedipine-sensitive ICa . The PKC-ßII antagonist LY379196, returned ICa amplitude to levels found in non-expresser myocytes. Increase in ICa was independent of Cav1.2-subunit mRNA levels as determined by quantitative RT-PCR. Thus, these data demonstrate that PKC-ß is a potent modulator of cardiac L-type calcium channels and that this specific isoform increases ICa in neonatal ventricular myocytes.




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