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J Biol Chem, Vol. 274, Issue 32, 22251-22256, August 6, 1999
-Adrenergic Receptor Signaling Precedes the
Development of Dilated Cardiomyopathy in Transgenic Mice with
Calsequestrin Overexpression
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From the Calsequestrin is a high capacity
Ca2+-binding protein in the junctional sarcoplasmic
reticulum that forms a quaternary complex with junctin, triadin, and
the ryanodine receptor. Transgenic mice with cardiac-targeted
calsequestrin overexpression show marked suppression of
Ca2+-induced Ca2+ release, myocyte hypertrophy,
and premature death by 16 weeks of age (Jones, L. R., Suzuki,
Y. J., Wang, W., Kobayashi, Y. M., Ramesh, V.,
Franzini-Armstrong, C., Cleemann, L., and Morad, M. (1998)
J. Clin. Invest. 101, 1385-1393). To investigate
whether alterations in intracellular Ca2+ trigger changes
in the Department of Medicine, University of North
Carolina, Chapel Hill, North Carolina 27599, Department of
Surgery, Duke University, Durham, North Carolina 27710, and
Krannert Institute of Cardiology and Department of
Medicine, Indiana University School of Medicine,
Indianapolis, Indiana 46202
-adrenergic receptor pathway, we studied calsequestrin
overexpressing transgenic mice at 7 and 14 weeks of age. As assessed by
echocardiography, calsequestrin mice at 7 weeks showed mild left
ventricular enlargement, mild decreased fractional shortening with
increased wall thickness. By 14 weeks, the phenotype progressed to
marked left ventricular enlargement and severely depressed systolic
function. Cardiac catheterization in calsequestrin mice revealed
markedly impaired -adrenergic receptor responsiveness in both 7- and
14- week mice. Biochemical analysis in 7- and 14-week mice showed a
significant decrease in total -adrenergic receptor density, adenylyl
cyclase activity, and the percent high affinity agonist binding, which
was associated with increased -adrenergic receptor kinase 1 levels.
Taken together, these data indicate that alterations in -adrenergic
receptor signaling precede the development of overt heart failure in
this mouse model of progressive cardiomyopathy.
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