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Department of Pharmacology and Cancer Biology (J.M.C., A.R.M.) and Department of Medicine (L.M., H.A.R., A.R.M.), Duke University Medical Center, Durham, North Carolina 27710
Address all correspondence and requests for reprints to: A. R. Means, Department of Pharmacology and Cancer Biology, Box 3813, Durham, North Carolina 27710. E-mail: means001{at}mc.duke.edu.
Signals transduced by the multifunctional calcium/calmodulin-dependent protein kinases (CaMKs), have been suggested to regulate the development of hypertrophy. We address the role of the three multifunctional CaMKs, CaMK I, II, and IV, in this process using transverse aortic constriction (TAC) to induce cardiac hypertrophy in mice. We find a 33% increase in total CaMK activity 7 d after TAC. However, there are no changes in the levels of CaMKI, which is expressed in the ventricles, or CaMKIV, which is not detectable in the ventricles. Moreover, mice null for the CaMKIV gene develop ventricular hypertrophy and induce the expression of selected hypertrophy marker mRNAs, indicating that CaMKIV is not required at any time during the development of hypertrophy. On the other hand, TAC does increase both mRNA and protein levels of specific isoforms of CaMKII derived from both 
and 
genes. Included among these isoforms are those that localize to both cytoplasm and nucleus. Collectively, the increased levels of CaMKII isoforms result in a constitutive increase in the Ca2+/calmodulin-independent activity of CaMKII in the ventricles. We conclude that CaMKII is the multifunctional CaMK most likely to mediate Ca2+- dependent protein phosphorylation events in response to TAC-induced cardiac hypertrophy.
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