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Articles in PresS, published online ahead of print February 13, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00435.2001
Submitted on September 10, 2001
Accepted on February 11, 2002
-actinin and dystrophin
1 Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT, USA
* To whom correspondence should be addressed. E-mail: barrydjohnson{at}telus.net.
The actin-binding proteins dystrophin and -actinin are members of a family of actin-binding proteins that may link the cytoskeleton to membrane proteins such as ion channels. Previous work demonstrated that the activity of Ca2+ channels can be regulated by agents that disrupt or stabilize the cytoskeleton. We employed immunohistochemical and electrophysiological techniques to investigate the potential regulation of cardiac L-type Ca2+ channel activity by dystrophin and -actinin in cardiac myocytes and in heterologous cells. Both actin binding proteins were found to colocalize with the Ca2+ channel in mouse cardiac myocytes and to modulate channel function. Inactivation of the Ca2+ channel in cardiac myocytes from mice lacking dystrophin (mdx mice) was reduced compared to that in wild-type myocytes, voltage-dependence of activation was shifted by 5 mV to more positive potentials, and stimulation by the ß-adrenergic pathway and the dihydropyridine agonist Bay K 8644 were increased. Further, heterologous coexpression of the Ca2+ channel with muscle, but not non-muscle, forms of -actinin in heterolgous cells was also found to reduce inactivation. As might be predicted from a reduction of Ca2+ channel inactivation, a prolongation of the mouse electrocardiogram QT was observed in mdx mice. These results suggest a combined role for dystrophin and -actinin in regulating the activity of the cardiac L-type Ca2+ channel and a potential mechanism for cardiac dysfunction in Duchenne and Becker muscular dystrophies.
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