FEBS Letters
Volume 583, Issue 22 , Pages 3600-3604, 19 November 2009

Essential role of TRPV2 ion channel in the sensitivity of dystrophic muscle to eccentric contractions

Edited by Gianni Cesareni

  • Nadège Zanou

      Affiliations

    • Laboratory of Cell Physiology, Institute of Neurosciences, Université catholique de Louvain, 55/40 av. Hippocrate, 1200 Brussels, Belgium
    • ,
  • Yuko Iwata

      Affiliations

    • Department of Molecular Physiology, National Cardiovascular Center Research Institute Suita, Osaka 565-8565, Japan
    • ,
  • Olivier Schakman

      Affiliations

    • Laboratory of Cell Physiology, Institute of Neurosciences, Université catholique de Louvain, 55/40 av. Hippocrate, 1200 Brussels, Belgium
    • ,
  • Jean Lebacq

      Affiliations

    • Laboratory of Cell Physiology, Institute of Neurosciences, Université catholique de Louvain, 55/40 av. Hippocrate, 1200 Brussels, Belgium
    • ,
  • Shigeo Wakabayashi

      Affiliations

    • Department of Molecular Physiology, National Cardiovascular Center Research Institute Suita, Osaka 565-8565, Japan
    • ,
  • Philippe Gailly

      Affiliations

    • Laboratory of Cell Physiology, Institute of Neurosciences, Université catholique de Louvain, 55/40 av. Hippocrate, 1200 Brussels, Belgium
    • Corresponding Author InformationCorresponding author. Fax: +32 2 7645580.

Received 4 September 2009; received in revised form 9 October 2009; accepted 12 October 2009. published online 19 October 2009.

Abstract 

Duchenne myopathy is a lethal disease due to the absence of dystrophin, a cytoskeletal protein. Muscles from dystrophin-deficient mice (mdx) typically present an exaggerated susceptibility to eccentric work characterized by an important force drop and an increased membrane permeability consecutive to repeated lengthening contractions. The present study shows that mdx muscles are largely protected from eccentric work-induced damage by overexpressing a dominant negative mutant of TRPV2 ion channel. This observation points out the role of TRPV2 channel in the physiopathology of Duchenne muscular dystrophy.

Keywords: Eccentric contraction, Calcium, TRPV2, Duchenne muscular dystrophy

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S0014-5793(09)00809-6

doi:10.1016/j.febslet.2009.10.033

FEBS Letters
Volume 583, Issue 22 , Pages 3600-3604, 19 November 2009

Article Tools

* Image Usage & Resolution