Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction
<p>Abstract</p> <p>Background</p> <p>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...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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BMC
2010-11-01
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| Series: | BMC Research Notes |
| Online Access: | http://www.biomedcentral.com/1756-0500/3/307 |
| _version_ | 1818806582154100736 |
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| author | Emond Mary J Bible Kenneth L Enns Linda C Ladiges Warren C |
| author_facet | Emond Mary J Bible Kenneth L Enns Linda C Ladiges Warren C |
| author_sort | Emond Mary J |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>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.</p> <p>Findings</p> <p>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.</p> <p>Conclusion</p> <p>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.</p> |
| first_indexed | 2024-12-18T19:12:03Z |
| format | Article |
| id | doaj.art-532a5942c8a9481c90cc199e42308b03 |
| institution | Directory Open Access Journal |
| issn | 1756-0500 |
| language | English |
| last_indexed | 2024-12-18T19:12:03Z |
| publishDate | 2010-11-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Research Notes |
| spelling | doaj.art-532a5942c8a9481c90cc199e42308b032022-12-21T20:56:13ZengBMCBMC Research Notes1756-05002010-11-013130710.1186/1756-0500-3-307Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunctionEmond Mary JBible Kenneth LEnns Linda CLadiges Warren C<p>Abstract</p> <p>Background</p> <p>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.</p> <p>Findings</p> <p>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.</p> <p>Conclusion</p> <p>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.</p>http://www.biomedcentral.com/1756-0500/3/307 |
| spellingShingle | Emond Mary J Bible Kenneth L Enns Linda C Ladiges Warren C Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction BMC Research Notes |
| title | Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction |
| title_full | Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction |
| title_fullStr | Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction |
| title_full_unstemmed | Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction |
| title_short | Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction |
| title_sort | mice lacking the cβ subunit of pka are resistant to angiotensin ii induced cardiac hypertrophy and dysfunction |
| url | http://www.biomedcentral.com/1756-0500/3/307 |
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