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    β1-Adrenergic Receptor and Sphingosine- 1-Phosphate Receptor 1 Reciprocal Down-Regulation Influences Cardiac Hypertrophic Response and Progression Toward Heart Failure: Protective Role of S1PR1 Cardiac Gene Therapy

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    Publication date
    2013-10-08
    Author
    Cannavo, A.
    Rengo, G.
    Liccardo, D.
    Pagano, G.
    Zincarelli, C.
    De Angelis, M.C.
    Puglia, R.
    Di Pietro, E.
    Rabinowitz, J.E.
    Barone, M.V.
    Cirillo, P.
    Trimarco, B.
    Palmer, Timothy M.
    Ferrara, N.
    Koch, W.J.
    Leosco, D.
    Rapacciuolo, A.
    Show allShow less
    Keyword
    Genetic therapy; Heart failure; Hypertrophy; Receptors; Adrenergic; Beta; Signal transduction
    Rights
    (c) 2013 The Authors. Full-text reproduced in accordance with the publisher's self-archiving policy.
    Peer-Reviewed
    Yes
    
    Metadata
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    Abstract
    The Sphingosine-1-phosphate receptor 1 (S1PR1) and β1-adrenergic receptor (β1AR) are G protein-coupled receptors (GPCRs) expressed in the heart. These two GPCRs have opposing actions on adenylyl cyclase due to differential G protein-coupling. Importantly, both of these receptors can be regulated by the actions of GPCR kinase-2 (GRK2), which triggers desensitization and down-regulation processes. Although, classical signaling paradigms suggest that simultaneous activation of β1ARs and S1PR1s in a myocyte would simply be opposing action on cAMP production, in this report we have uncovered a direct interaction between these two receptors with a regulatory involvement of GRK2. In HEK293 cells overexpressing both β1AR and S1PR1, we demonstrate that β1AR down-regulation can occur after sphingosine 1-phosphate (S1PR1 agonist) stimulation while S1PR1 down-regulation can be triggered by isoproterenol (βAR agonist) treatment. This cross-talk between these two distinct GPCRs appears to have physiological significance since they interact and show reciprocal regulation in mouse hearts undergoing chronic βAR stimulation and also in a rat model of post-ischemic heart failure (HF). We demonstrate that restoring cardiac plasma membrane levels of S1PR1 produce beneficial effects counterbalancing deleterious β1AR overstimulation in HF.
    URI
    http://hdl.handle.net/10454/7923
    Version
    Accepted Manuscript
    Citation
    Cannavo A, Rengo G, Liccardo D et al (2013) β1-Adrenergic Receptor and Sphingosine- 1-Phosphate Receptor 1 Reciprocal Down-Regulation Influences Cardiac Hypertrophic Response and Progression Toward Heart Failure: Protective Role of S1PR1 Cardiac Gene Therapy. Circulation. 128(15): 1612–1622.
    Link to publisher’s version
    http://dx.doi.org/10.1161/CIRCULATIONAHA.113.002659
    Type
    Article
    Collections
    Life Sciences Publications

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