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January 1, 2014Journal of Cell ScienceOpen Access

Genetic ablation of PDE4B disrupted β1AR-induced cAMP transients at the sarcolemma, augmenting local cAMP/PKA signals and leading to an increased intracellular Ca(2+) level and contraction rate.

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Population

Cardiomyocytes (model of genetic ablation of PDE4B)

Comparison

Genetic ablation of PDE4B and application of PKA… vs Control cardiomyocytes (implied)

Design

Preclinical

Authors

DMDelphine MikaWRWito RichterRWRuth E. Westenbroek

Discussion

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Overview

PDE4B ablation findings in rodent cardiomyocytes support compartmentalized signaling models; leaves open human therapeutic relevance.

Structured PICO

P
Population
Cardiomyocytes (model of genetic ablation of PDE4B)
I
Intervention
Genetic ablation of PDE4B and application of PKA inhibitors
C
Comparator
Control cardiomyocytes (implied)
O
Outcome
β-adrenergic (βAR)-induced cAMP transients at the sarcolemma, PKA-mediated phosphorylation patterns, intracellular Ca(2+) level, and contraction ratesurrogate

PDE4B mediates a crucial PKA-dependent negative feedback loop that controls β1AR-dependent cAMP signals in a restricted subsarcolemmal domain of cardiomyocytes.

Cite This Study

Mika et al. (2014) studied this question.

synapsesocial.com/papers/6a8b9d42e76aab3312338340https://doi.org/10.1242/jcs.140251
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