August 26, 2005Circulation ResearchOpen Access

Enhanced Functional Gap Junction Neoformation by Protein Kinase A–Dependent and Epac-Dependent Signals Downstream of cAMP in Cardiac Myocytes

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Structured PICO

Population

Cardiac myocytes

Intervention

PKA-specific activator N6-benzoyladenosine-3',5'-cyclic monophosphate (6Bnz), Epac-specific activator 8-(4-chlorophenylthio)-2'-O-methyladenosine-3',5'-cyclic monophosphate (8CPT), and overexpression of Rap1GAP1b

Outcome

Gap junction gating function (measured by microinjected dye transfer) and accumulation of connexin43 (measured by quantitative immunostaining)surrogate

PKA and Epac signals downstream of cAMP cooperatively enhance functional gap junction neoformation in cardiac myocytes.

Discussion

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Implication

PKA/Epac modulation may enhance myocyte coupling; leaves open whether these pathways improve conduction or reduce arrhythmias in vivo.

Cite This Study

Somekawa et al. (2005) studied this question.

synapsesocial.com/papers/6a708e53e71d69abee08af65 https://doi.org/10.1161/01.res.0000183880.49270.f9

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Enhanced Functional Gap Junction Neoformation by Protein Kinase A–Dependent and Epac-Dependent Signals Downstream of cAMP in Cardiac Myocytes

Structured PICO

Discussion

Implication

Cite This Study

Enhanced Functional Gap Junction Neoformation by Protein Kinase A–Dependent and Epac-Dependent Signals Downstream of cAMP in Cardiac Myocytes

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider