| First Author | Iwaya S | Year | 2014 |
| Journal | Int Heart J | Volume | 55 |
| Issue | 2 | Pages | 165-8 |
| PubMed ID | 24632966 | Mgi Jnum | J:307885 |
| Mgi Id | MGI:6725962 | Doi | 10.1536/ihj.13-268 |
| Citation | Iwaya S, et al. (2014) Phosphodiesterase 3A1 protects the heart against angiotensin II-induced cardiac remodeling through regulation of transforming growth factor-beta expression. Int Heart J 55(2):165-8 |
| abstractText | Accumulating evidence suggests that there are direct interactions between beta-adrenergic and angiotensin II signaling pathways, and beta-blockers protect the heart against angiotensin II-induced cardiac remodeling. Phosphodiesterase 3A (PDE3A) regulates beta-adrenergic receptor/protein kinase A signaling by metabolizing cAMP. Therefore, we hypothesized that overexpressed PDE3A has cardioprotective effects against angiotensin II-induced cardiac remodeling by regulating angiotensin II signaling. In the present study, we used transgenic mice with cardiac-specific overexpressed PDE3A1. We showed that continuous administration of angiotensin II caused cardiac hypertrophy in the wild-type mouse heart, but not in the transgenic mouse heart. Angiotensin II induced cardiac fibrosis in both wild-type and transgenic mice, but the extent of fibrosis was less in transgenic mice compared to wild-type mice. Moreover, basal expression levels of transforming growth factor-beta were lower in transgenic mouse hearts, and it remained at lower levels after angiotensin II stimulation. These findings suggest that PDE3A protects the heart from angiotensin II-induced cardiac remodeling through its modulation of the functional connection between angiotensin II and transforming growth factor-beta. |
