• Medientyp: E-Artikel
  • Titel: Cardiac Voltage-Gated Sodium Channel Na v 1.5 Is Regulated by Nedd4-2 Mediated Ubiquitination
  • Beteiligte: van Bemmelen, Miguel X.; Rougier, Jean-Sébastien; Gavillet, Bruno; Apothéloz, Florine; Daidié, Dorothée; Tateyama, Michihiro; Rivolta, Ilaria; Thomas, Marc A.; Kass, Robert S.; Staub, Olivier; Abriel, Hugues
  • Erschienen: Ovid Technologies (Wolters Kluwer Health), 2004
  • Erschienen in: Circulation Research
  • Sprache: Englisch
  • DOI: 10.1161/01.res.0000136816.05109.89
  • ISSN: 0009-7330; 1524-4571
  • Schlagwörter: Cardiology and Cardiovascular Medicine ; Physiology
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  • Beschreibung: <jats:p> Na <jats:sub>v</jats:sub> 1.5, the cardiac isoform of the voltage-gated Na <jats:sup>+</jats:sup> channel, is critical to heart excitability and conduction. However, the mechanisms regulating its expression at the cell membrane are poorly understood. The Na <jats:sub>v</jats:sub> 1.5 C-terminus contains a PY-motif (xPPxY) that is known to act as binding site for Nedd4/Nedd4-like ubiquitin-protein ligases. Because Nedd4-2 is well expressed in the heart, we investigated its role in the ubiquitination and regulation of Na <jats:sub>v</jats:sub> 1.5. Yeast two-hybrid and GST-pulldown experiments revealed an interaction between Na <jats:sub>v</jats:sub> 1.5 C-terminus and Nedd4-2, which was abrogated by mutating the essential tyrosine of the PY-motif. Ubiquitination of Na <jats:sub>v</jats:sub> 1.5 was detected in both transfected HEK cells and heart extracts. Furthermore, Nedd4-2–dependent ubiquitination of Na <jats:sub>v</jats:sub> 1.5 was observed. To test for a functional role of Nedd4-2, patch-clamp experiments were performed on HEK cells expressing wild-type and mutant forms of both Na <jats:sub>v</jats:sub> 1.5 and Nedd4-2. Na <jats:sub>v</jats:sub> 1.5 current density was decreased by 65% upon Nedd4-2 cotransfection, whereas the PY-motif mutant channels were not affected. In contrast, a catalytically inactive Nedd4-2 had no effect, indicating that ubiquitination mediates this downregulation. However, Nedd4-2 did not alter the whole-cell or the single channel biophysical properties of Na <jats:sub>v</jats:sub> 1.5. Consistent with the functional findings, localization at the cell periphery of Na <jats:sub>v</jats:sub> 1.5-YFP fusion proteins was reduced upon Nedd4-2 coexpression. The Nedd4-1 isoform did not regulate Na <jats:sub>v</jats:sub> 1.5, suggesting that Nedd4-2 is a specific regulator of Na <jats:sub>v</jats:sub> 1.5. These results demonstrate that Na <jats:sub>v</jats:sub> 1.5 can be ubiquitinated in heart tissues and that the ubiquitin-protein ligase Nedd4-2 acts on Na <jats:sub>v</jats:sub> 1.5 by decreasing the channel density at the cell surface. </jats:p>
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