What question did this study set out to answer?

The aim is to assess how the null mutation of connexin43 affects electrical wave propagation during mouse embryonic development.

June 8, 2001Circulation Research

Null Mutation of Connexin43 Causes Slow Propagation of Ventricular Activation in the Late Stages of Mouse Embryonic Development

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Population

Isolated Cx43 null mutated (Cx43(-/-)), heterozygous (Cx43(+/-)), and wild-type (WT) mouse embryos

Comparison

Connexin43 (Cx43) null mutation vs Wild-type and heterozygous (Cx43) mouse embryos

Design

Preclinical

Authors

DVDhananjay VaidyaPreventive Cardiology HTHouman TamaddonAugusta University CLCecilia W. LoUniversity of Pittsburgh

Discussion

Member takes

Implication

Cx43 essential for embryonic ventricular conduction; extends developmental models but leaves open human arrhythmia relevance.

Key Points

The aim is to assess how the null mutation of connexin43 affects electrical wave propagation during mouse embryonic development.
Isolated left and right ventricles from Cx43 null, heterozygous, and wild-type embryos were examined.
High-resolution mapping of voltage-sensitive dye fluorescence was used to evaluate electrical wave propagation.
Conduction velocities were measured at different embryonic stages (12.5, 15.5, and 17.5 dpc).
At 15.5 dpc, Cx43(-/-) ventricles demonstrated a significant reduction in conduction velocity to 2.2 cm/sec compared to 9.9 cm/sec in control groups (P<0.005).
At 17.5 dpc, conduction velocities in Cx43(-/-) were 1.1 cm/sec for RV and 1.7 cm/sec for LV versus 8.4 cm/sec and 10.1 cm/sec in wild-type, respectively (P<0.005).
Neonatal knockout hearts exhibited arrhythmias both in vivo and ex vivo.

Structured PICO

Population

Isolated Cx43 null mutated (Cx43(-/-)), heterozygous (Cx43(+/-)), and wild-type (WT) mouse embryos

Intervention

Connexin43 (Cx43) null mutation

Comparator

Wild-type (WT) and heterozygous (Cx43(+/-)) mouse embryos

Outcome

Electrical wave propagation velocity in the left (LV) and right (RV) ventricles measured using high-resolution mapping of voltage-sensitive dye fluorescencesurrogate

Connexin43 is essential for maintaining normal electrical wave propagation and heart rhythm in the late stages of mouse embryonic development and postnatal life.

Cite This Study

Vaidya et al. (2001) studied this question.

synapsesocial.com/papers/69dd2e777808b00a4799b643 https://doi.org/10.1161/hh1101.091107

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Null Mutation of Connexin43 Causes Slow Propagation of Ventricular Activation in the Late Stages of Mouse Embryonic Development

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Null Mutation of Connexin43 Causes Slow Propagation of Ventricular Activation in the Late Stages of Mouse Embryonic Development

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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