August 3, 2007Circulation ResearchOpen Access

Connexin43 Remodeling Caused by Inhibition of Plakophilin-2 Expression in Cardiac Cells

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Population

Cardiac cells (ventricular myocytes and epicardium-derived cells) obtained from neonatal rat hearts

Design

Preclinical

Authors

EOEva M. OxfordCornell University HMHassan MusaNorfolk State University KMKaren MaassNew York University

Discussion

Member takes

Implication

Hypothesis-generating for PKP2-Cx43 disruption in ARVC arrhythmogenesis; human studies needed before clinical translation.

Structured PICO

Population

Cardiac cells (ventricular myocytes and epicardium-derived cells) obtained from neonatal rat hearts

Intervention

RNA silencing technology to decrease the expression of plakophilin-2 (PKP2)

Outcome

Content, distribution, and function of connexin43 (Cx43) gap junctionssurrogate

Inhibition of PKP2 expression disrupts Cx43 gap junctions, providing a molecular mechanism for arrhythmogenesis in arrhythmogenic right ventricular cardiomyopathy.

Cite This Study

Oxford et al. (2007) studied this question.

synapsesocial.com/papers/69fa8a569fa336b96d47d9a9 https://doi.org/10.1161/circresaha.107.154252

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Connexin43 Remodeling Caused by Inhibition of Plakophilin-2 Expression in Cardiac Cells

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Connexin43 Remodeling Caused by Inhibition of Plakophilin-2 Expression in Cardiac Cells

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider