Marie Allouis

Publications (4)19.29 Total impact

• Source

  Available from: Isabelle Baró

  Article: 14-3-3 is a regulator of the cardiac voltage-gated sodium channel Nav1.5.

  Marie Allouis, Françoise Le Bouffant, Ronald Wilders, David Péroz, Jean-Jacques Schott, Jacques Noireaud, Hervé Le Marec, Jean Mérot, Denis Escande, Isabelle Baró
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  ABSTRACT: The voltage-sensitive Na(+) channel Na(v)1.5 plays a crucial role in generating and propagating the cardiac action potential and its dysfunction promotes cardiac arrhythmias. The channel takes part into a large molecular complex containing regulatory proteins. Thus, factors that modulate its biosynthesis, localization, activity, and/or degradation are of great interest from both a physiological and pathological standpoint. Using a yeast 2-hybrid screen, we unveiled a novel partner, 14-3-3eta, interacting with the Na(v)1.5 cytoplasmic I interdomain. The interaction was confirmed by coimmunoprecipitation of 14-3-3 and full-length Na(v)1.5 both in COS-7 cells expressing recombinant Na(v)1.5 and in mouse cardiac myocytes. Using immunocytochemistry, we also found that 14-3-3 and Na(v)1.5 colocalized at the intercalated discs. We tested the functional link between Na(v)1.5 and 14-3-3eta using the whole-cell patch-clamp configuration. Coexpressing Na(v)1.5, the beta1 subunit and 14-3-3eta induced a negative shift in the inactivation curve of the Na(+) current, a delayed recovery from inactivation, but no changes in the activation curve or in the current density. The negative shift was reversed, and the recovery from inactivation was normalized by overexpressing the Na(v)1.5 cytoplasmic I interdomain interacting with 14-3-3eta. Reversal was also obtained with the dominant negative R56,60A 14-3-3eta mutant, suggesting that dimerization of 14-3-3 is needed for current regulation. Computer simulations suggest that the absence of 14-3-3 could exert proarrhythmic effects on cardiac electrical restitution properties. Based on these findings, we propose that the 14-3-3 protein is a novel component of the cardiac Na(+) channel acting as a cofactor for the regulation of the cardiac Na(+) current.
  Circulation Research 07/2006; 98(12):1538-46. · 9.49 Impact Factor
• Article: Progressive cardiac conduction defect is the prevailing phenotype in carriers of a Brugada syndrome SCN5A mutation.

  Vincent Probst, Marie Allouis, Frederic Sacher, Sabine Pattier, Dominique Babuty, Philipe Mabo, Jacques Mansourati, Jacques Victor, Jean-Michel Nguyen, Jean-Jacques Schott, Pierre Boisseau, Denis Escande, Hervé Le Marec
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  ABSTRACT: Loss-of-function mutations in the SCN5A gene encoding the cardiac sodium channel are responsible for Brugada syndrome (BS) and also for progressive cardiac conduction disease (inherited Lenègre disease). In an attempt to clarify the frontier between these two entities, we have characterized cardiac conduction defect and its evolution with aging in a cohort of 78 patients carrying a SCN5A mutation linked to Brugada syndrome. Families were included in the study if a SCN5A mutation was identified in a BS proband and if at least two family members were mutation carriers. Sixteen families met the study criteria, representing 78 carriers. Resting ECG showed a spontaneous BS ECG pattern in 28 of 78 (36%) gene carriers. Intraventricular conduction anomalies were identified in 59 of 78 gene carriers including complete (17) or incomplete (24) right bundle branch block, right bundle branch block plus hemiblock (6), left bundle branch block (1), hemiblock (1), and parietal block (10). PR and QRS duration were longer in the gene carrier cohort in comparison with their relatives carrying no mutation. Finally, in the gene carrier cohort conduction defect progressively aggravated with aging leading in five occasions to pacemaker implantations. The present study shows that the most common phenotype of gene carriers of a BS-type SCN5A mutation is progressive cardiac conduction defects similar to the Lenègre disease phenotype. In consequence, we propose that carriers of a SCN5A mutation need a clinical and ECG follow-up because of the risk associated with severe conduction defects.
  Journal of Cardiovascular Electrophysiology 04/2006; 17(3):270-5. · 3.06 Impact Factor
• Article: Unusual clinical presentation in a family with catecholaminergic polymorphic ventricular tachycardia due to a G14876A ryanodine receptor gene mutation.

  Marie Allouis, Vincent Probst, Philippe Jaafar, Jean-Jacques Schott, Hervé Le Marec
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  ABSTRACT: A family was identified, of whom which 11 members were carriers of the G14876A ryanodine 2 receptor mutation. All but 1 were symptomatic at the time of the study. Exercise testing showed bidirectional or polymorphic arrhythmias in 4 patients, whereas in 5 patients, it showed monomorphic or rare minor polymorphic ventricular arrhythmias. Two young patients died suddenly at rest while asleep. This study demonstrates that arrhythmias occurring during exercise stress testing in patients affected by catecholaminergic polymorphic ventricular tachycardia (CPVT) could be minor even in very symptomatic patients. The diagnosis of CPVT must be considered in these patients with a familial history of typical CPVT.
  The American Journal of Cardiology 04/2005; 95(5):700-2. · 3.37 Impact Factor
• Article: Cosegregation of the Marfan syndrome and the long QT syndrome in the same family leads to a severe cardiac phenotype.

  Vincent Probst, Marie Allouis, Florence Kyndt, Gilles Lande, Jean-Noël Trochu, Jean-Jacques Schott, Hervé Le Marec
  The American Journal of Cardiology 04/2003; 91(5):635-7. · 3.37 Impact Factor