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activation induces dichotomous cardiac phenotypes
and modulates PKC-RACK interactions and RACK expression
1 Division of Cardiology, Department of Medicine, and 2 Department of Physiology and Biophysics, University of Louisville, Louisville, Kentucky 40292
Receptors for
activated C kinase (RACKs) have been shown to facilitate activation of
protein kinase C (PKC). However, it is unknown whether PKC activation
modulates RACK protein expression and PKC-RACK interactions. This issue
was studied in two PKC
transgenic lines exhibiting dichotomous
cardiac phenotypes: one exhibits increased resistance to myocardial
ischemia (cardioprotected phenotype) induced by a modest
increase in PKC activity (228 ± 23% of control), whereas the
other exhibits cardiac hypertrophy and failure (hypertrophied
phenotype) induced by a marked increase in PKC activity (452 ± 28% of control). Our data demonstrate that activation of PKC modulates
the expression of RACK isotypes and PKC-RACK interactions in a PKC
activity- and dosage-dependent fashion. We found that, in mice
displaying the cardioprotected phenotype, activation of PKC enhanced
RACK2 expression (178 ± 13% of control) and particulate
PKC-RACK2 protein-protein interactions (178 ± 18% of
control). In contrast, in mice displaying the hypertrophied phenotype,
there was not only an increase in RACK2 expression (330 ± 33% of
control) and particulate PKC-RACK2 interactions (154 ± 14% of
control) but also in RACK1 protein expression (174 ± 10% of
control). Most notably, PKC-RACK1 interactions were identified in
this line. With the use of transgenic mice expressing a dominant
negative PKC, we found that the changes in RACK expression as well
as the attending cardiac phenotypes were dependent on PKC activity.
Our observations demonstrate that RACK expression is dynamically
regulated by PKC and suggest that differential patterns of
PKC-RACK interactions may be important determinants of
PKC-dependent cardiac phenotypes.
protein-protein interactions; cardiac phenotypes; protein kinase C; transgenic mouse; receptors for activated C kinase
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