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Cardiovascular Research Advance Access first published online on August 13, 2009
This version [Corrected Proof] published online on September 4, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp280
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Connexin 30 is expressed in the mouse sino-atrial node and modulates heart rate

Daniel Gros1,*, Magali Théveniau-Ruissy1, Monique Bernard2, Thierry Calmels3, Frank Kober2, Goran Söhl4,{dagger}, Klaus Willecke4, Joël Nargeot5, Habo J. Jongsma6 and Matteo E. Mangoni5

1 Institut de Biologie du Développement de Marseille-Luminy (UMR CNRS 6216), Université de la Méditerranée, Campus Scientifique de Luminy, case 907, Avenue de Luminy, 13288 Marseille, France
2 Centre de Résonance Magnétique Biologique et Médicale (UMR CNRS 6612), Université de la Méditerranée, Marseille, France
3 Bioprojet-Biotech, Saint Grégoire, France
4 Institut für Genetik, Abteilung Molekulargenetik, Universität Bonn, Bonn, Germany
5 Institut de Génomique Fonctionnelle (UMR CNRS 5203, Unité INSERM 661), Universités de Montpellier I et II, Département de Physiologie, Montpellier, France
6 Department of Medical Physiology, University Medical Center, Utrecht, The Netherlands

* Corresponding author. Tel: +33 491 26 97 33, Fax: +33 491 26 97 26, Email: daniel.gros{at}ibdml.univ-mrs.fr

Aims: This study aimed at characterizing expression and the functional role of the Gjb6 gene, encoding for connexin 30 (Cx30) protein, in the adult mouse heart.

Methods and results: The expression of the Gjb6 gene in the mouse heart was investigated by RT–PCR and sequencing of amplified cDNA fragments. The sites of Gjb6 expression were identified in the adult heart using transgenic mice with reporter genes (Cx30LacZ/LacZ and Cx30LacZ/LacZ/Cx40EGFP/EGFP mice), as well as anti-HCN4 (hyperpolarization activated cyclic nucleotide-gated potassium channel 4) or anti-connexin antibodies. Cine-magnetic resonance imaging and telemetric ECG recordings were used to evaluate the impact of Cx30 deficiency on cardiac physiology. Gjb6 was shown to be expressed in the sinoatrial (SA) node of the adult mouse heart. Eighty from 100 nuclei on average were LacZ-positive in the SA node of Cx30LacZ/LacZ mice. No significant LacZ expression was seen in other cardiac tissues. Cx30 protein was identified in low abundance in the SA node of wild-type mice, as indicated by immunofluorescence experiments. Telemetric ECG recordings indicated that Cx30-deficient mice displayed a mean daily heart rate (HR) that was 9% faster than that measured in control mice (572 ± 38 b.p.m. vs. 524 ± 23, P < 0.05). This moderate tachycardia was still observed after inhibition of the autonomic nervous system, demonstrating that Cx30 deficiency resulted in changes in the intrinsic electrical properties of the SA node. Consistent with this hypothesis, Cx30LacZ/LacZ displayed a significant reduction of SDNN (standard deviation of the interbeat interval) compared with control mice. Increase of both the cardiac index (20%) and the end-diastolic volume to body weight ratio (16%) with no deficiency in ejection fraction or stroke volume were observed in mutant mice. An increase in cardiac index was interpreted as being a direct consequence of high HR, whereas large end-diastolic volume may be an indirect consequence of prolonged high HR.

Conclusion: Cx30 is functionally expressed, in low abundance, in the SA node of the adult mouse heart where it participates in HR regulation.

KEYWORDS Gjb6 gene; Connexin 30; Gap junction; Intercellular coupling; Sinoatrial node; Pacemaker; Mouse heart; Heart rate

Time for primary review: 21 days

{dagger} Present address: Martinus Gymnasium, Martinusstraße, 53541 Linz, Germany


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