| First Author | Tsunematsu T | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 458 |
| Issue | 3 | Pages | 531-5 |
| PubMed ID | 25677623 | Mgi Jnum | J:220489 |
| Mgi Id | MGI:5634866 | Doi | 10.1016/j.bbrc.2015.01.149 |
| Citation | Tsunematsu T, et al. (2015) Coupling of beta1-adrenergic receptor to type 5 adenylyl cyclase and its physiological relevance in cardiac myocytes. Biochem Biophys Res Commun 458(3):531-5 |
| abstractText | Myocardial beta-adrenergic receptor (beta-AR) beta1- and beta2-subtypes are highly homologous, but play opposite roles in cardiac apoptosis and heart failure, as do cardiac adenylyl cyclase (AC) subtypes 5 (AC5) and 6 (AC6): beta1-AR and AC5 promote cardiac remodeling, while beta2-AR and AC6 activate cell survival pathways. However, the mechanisms involved remain poorly understood. We hypothesized that AC5 is coupled preferentially to beta1-AR rather than beta2-AR, and we examined this idea by means of pharmacological and genetic approaches. We found that selective inhibition of AC5 with 2'5'-dideoxyadenosine significantly suppressed cAMP accumulation and cardiac apoptosis induced by selective beta1-AR stimulation, but had no effect on cAMP accumulation and cardiac apoptosis in response to selective beta2-AR stimulation. The results of selective stimulation of beta1-AR and beta2-AR in neonatal cardiac myocytes prepared from wild-type and AC5-knockout mice were also consistent with the idea that beta1-AR selectively couples with AC5. We believe these results are helpful for understanding the mechanisms underlying the different roles of AR subtypes in healthy and diseased hearts. |
