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Published on: September 28, 2015
Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction
Linda C Enns1, Kenneth L Bible, Mary J Emond
1Departments of Comparative Medicine, Physiology and Biophysics, and Biostatistics, University of Washington, Seattle, WA, 98195, USA. wladiges@u.washington.edu.
Background:
PKA is a ubiquitous, multi-subunit cellular kinase that regulates a number of different physiological responses in response to cAMP, including metabolism, cell division, and cardiac function. Numerous studies have implicated altered PKA signaling in cardiac dysfunction. Recently, it has been shown that mice lacking the catalytic β subunit of PKA (PKA Cβ) are protected from age-related problems such as weight gain and enlarged livers, and we hypothesized that these mice might also be resistant to cardiomyopathy.
Findings:
Angiotensin II (ang II) induced hypertension in both PKA Cβ null mice and their WT littermates. However, PKA Cβ null mice were resistant to a number of ang II-induced, cardiopathological effects observed in the WT mice, including hypertrophy, decreased diastolic performance, and enlarged left atria.
Conclusion:
The Cβ subunit of PKA plays an important role in angiotensin-induced cardiac dysfunction. The Cβ null mouse highlights the potential of the PKA Cβ subunit as a pharmaceutical target for hypertrophic cardiac disease.
Insights
Mice lacking the protein kinase A catalytic beta subunit (PKA Cβ) showed resistance to angiotensin II-induced cardiac dysfunction. This suggests PKA Cβ is a potential therapeutic target for hypertrophic cardiac disease.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Protein kinase A (PKA) is a key regulator of cellular functions, including cardiac function.
- Altered PKA signaling is linked to cardiac dysfunction.
- Mice lacking the PKA catalytic beta subunit (PKA Cβ) are protected from certain age-related issues.
Purpose of the Study:
- To investigate the role of PKA Cβ in angiotensin II-induced cardiac dysfunction.
- To determine if PKA Cβ null mice are resistant to cardiomyopathy.
Main Methods:
- Induction of hypertension using Angiotensin II in PKA Cβ null mice and wild-type littermates.
- Assessment of cardiac function and pathological changes.
Main Results:
- Both PKA Cβ null and WT mice developed hypertension in response to Angiotensin II.
- PKA Cβ null mice exhibited resistance to Angiotensin II-induced cardiac hypertrophy.
- PKA Cβ null mice showed preserved diastolic performance and reduced left atrial enlargement compared to WT mice.
Conclusions:
- The PKA Cβ subunit is crucial in the development of Angiotensin II-induced cardiac dysfunction.
- Targeting the PKA Cβ subunit may offer a therapeutic strategy for hypertrophic cardiac disease.
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