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Updated: Aug 14, 2026
Transverse Aortic Constriction in Mice
Published on: April 21, 2010
PKC-beta is not necessary for cardiac hypertrophy
B B Roman1, D L Geenen, M Leitges
1Section of Cardiology, Department of Medicine, University of Illinois at Chicago, Illinois 60612, USA. broman@uic.edu
Abstract:
Studies in human and rodent models have shown that activation of protein kinase C-beta (PKC-beta) is associated with the development of pathological hypertrophy, suggesting that ablation of the PKC-beta pathway might prevent or reverse cardiac hypertrophy. To explore this, we studied mice with targeted disruption of the PKC-beta gene (knockout, KO). There were no detectable differences in expression or distribution of other PKC isoforms between the KO and control hearts as determined by Western blot analysis. Baseline hemodynamics were measured using a closed-chest preparation and there were no differences in heart rate and arterial or left ventricular pressure. Mice were subjected to two independent hypertrophic stimuli: phenylephrine (Phe) at 20 mg x kg(-1) x day(-1) sq infusion for 3 days, and aortic banding (AoB) for 7 days. KO animals demonstrated an increase in heart weight-to-body weight ratio (Phe, 4.3 +/- 0.6 to 6.1 +/- 0.4; AoB, 4.0 +/- 0.1 to 5.8 +/- 0.7) as well as ventricular upregulation of atrial natriuretic factor mRNA analogous to those seen in control animals. These results demonstrate that PKC-beta expression is not necessary for the development of cardiac hypertrophy nor does its absence attenuate the hypertrophic response.
Insights
Ablating protein kinase C-beta (PKC-beta) did not prevent cardiac hypertrophy in mice. These findings indicate that the PKC-beta pathway is not essential for developing or attenuating cardiac hypertrophy.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Physiology
Background:
- Protein kinase C-beta (PKC-beta) activation is linked to pathological cardiac hypertrophy in human and rodent models.
- Targeting the PKC-beta pathway is a potential strategy to prevent or reverse cardiac hypertrophy.
Purpose of the Study:
- To investigate the necessity of PKC-beta in the development of cardiac hypertrophy.
- To determine if PKC-beta deficiency attenuates the hypertrophic response to stimuli.
Main Methods:
- Studied gene knockout (KO) mice lacking the PKC-beta gene.
- Assessed cardiac hypertrophy using phenylephrine (Phe) infusion and aortic banding (AoB) models.
- Measured heart weight-to-body weight ratio and atrial natriuretic factor mRNA levels.
Main Results:
- No significant differences in baseline hemodynamics or other PKC isoform expression between KO and control mice.
- PKC-beta KO mice exhibited cardiac hypertrophy in response to both Phe and AoB stimuli, similar to control animals.
- Ventricular atrial natriuretic factor mRNA was upregulated in KO animals, indicating a hypertrophic response.
Conclusions:
- PKC-beta expression is not required for the development of cardiac hypertrophy.
- The absence of PKC-beta does not attenuate the cardiac hypertrophic response to pharmacological or mechanical stress.
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