Axial stretch-dependent cation entry in dystrophic cardiomyopathy: Involvement of several TRPs channels

Cell Calcium
E AguettazS Sebille

Abstract

In Duchenne muscular dystrophy (DMD), deficiency of the cytoskeletal protein dystrophin leads to well-described defects in skeletal muscle but also to dilated cardiomyopathy (DCM). In cardiac cells, the subsarcolemmal localization of dystrophin is thought to protect the membrane from mechanical stress. The dystrophin deficiency leads to membrane instability and a high stress-induced Ca(2+) influx due to dysregulation of sarcolemmal channels such as stretch-activated channels (SACs). In this work divalent cation entry has been explored in isolated ventricular Wild Type (WT) and mdx cardiomyocytes in two different conditions: at rest and during the application of an axial stretch. At rest, our results suggest that activation of TRPV2 channels participates to a constitutive basal cation entry in mdx cardiomyocytes.Using microcarbon fibres technique, an axial stretchwas applied to mimic effects of physiological conditions of ventricular filling and study on cation influx bythe Mn(2+)-quenching techniquedemonstrated a high stretch-dependentcationic influx in dystrophic cells, partially due to SACs. Involvement of TRPs channels in this excessive Ca(2+) influx has been investigated using specific modulators and demonstratedboth sarcol...Continue Reading

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Citations

Jan 22, 2019·Nature Reviews. Cardiology·Thomas HofRomain Guinamard
Dec 26, 2018·The Journal of Physiology·Humberto C JocaGeorge S B Williams
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May 27, 2017·Progress in Biophysics and Molecular Biology·Elizabeth AguettazStéphane Sebille
Jun 7, 2021·The Journal of Thoracic and Cardiovascular Surgery·Aya KimuraTakashi Mori

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