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- W76870306 abstract "We have shown that inhibition of the cAMP-specific type 4 cyclic nucleotide phosphodiesterases (PDE4s) modifies beta-adrenergic signaling in mouse neonatal cardiac myocytes. In the present study, we further elucidated the role of individual PDE4 variants in the control of b1- and b2-adrenergic receptor (b1-AR and b2-AR) signaling. Stimulation of b2-AR resulted in a selective PKA-mediated activation of the PDE4D splice variant PDE4D5. Conversely, the variant PDE4D8 was predominantly activated by PKA upon b1-AR stimulation. Cyclic AMP-hydrolyzing (PDE) activity was co-immunoprecipiated with bARs from extracts of myocytes overexpressing b1-AR or b2-AR. This activity is due to PDE4D, because it was sensitive to PDE4-selective inhibitors and PDE activity was still recovered when cells deficient in PDE4A or PDE4B but not PDE4D were used. Moreover, the physical association of PDE4D variants and b-ARs was reproduced by co-IPs of recombinant PDE4D splice variants with b1- and b2-AR. Importantly, treatment with b-adrenergic agonists such as Isoproterenol diminished the PDE4D/b-AR co-IP indicating that this complex is dynamically regulated by b-AR signaling. Taken together, our results indicate that distinct PDE4D splice variants form macromolecular signaling complexes with and control the cAMP signals from b1- and b2-ARs. This research was supported by NIH grants HD20788 to M.C. and HL71078-01 to B.K." @default.
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- W76870306 date "2007-01-01" @default.
- W76870306 modified "2023-10-15" @default.
- W76870306 title "Distinct PDE4D splice variants regulate beta‐adrenergic signaling in neonatal mouse cardiac myocytes" @default.
- W76870306 doi "https://doi.org/10.1096/fasebj.21.6.a997-b" @default.
- W76870306 hasPublicationYear "2007" @default.
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