Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes

Aims Long-QT syndromes (LQTS) are mostly autosomal-dominant congenital disorders associated with a 1:1000 mutation frequency, cardiac arrest, and sudden death. We sought to use cardiomyocytes derived from human-induced pluripotency stem cells (hiPSCs) as an in vitro model to develop and evaluate gen...

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Main Authors: Matsa, Elena, Dixon, James E., Medway, Christopher, Georgiou, Orestis, Patel, Minal J., Morgan, Kevin, Kemp, Paul J., Staniforth, Andrew, Mellor, Ian, Denning, Chris
Format: Article
Published: Oxford University Press 2013
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Online Access:https://eprints.nottingham.ac.uk/2664/
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author Matsa, Elena
Dixon, James E.
Medway, Christopher
Georgiou, Orestis
Patel, Minal J.
Morgan, Kevin
Kemp, Paul J.
Staniforth, Andrew
Mellor, Ian
Denning, Chris
author_facet Matsa, Elena
Dixon, James E.
Medway, Christopher
Georgiou, Orestis
Patel, Minal J.
Morgan, Kevin
Kemp, Paul J.
Staniforth, Andrew
Mellor, Ian
Denning, Chris
author_sort Matsa, Elena
building Nottingham Research Data Repository
collection Online Access
description Aims Long-QT syndromes (LQTS) are mostly autosomal-dominant congenital disorders associated with a 1:1000 mutation frequency, cardiac arrest, and sudden death. We sought to use cardiomyocytes derived from human-induced pluripotency stem cells (hiPSCs) as an in vitro model to develop and evaluate gene-based therapeutics for the treatment of LQTS. Methods and results We produced LQTS-type 2 (LQT2) hiPSC cardiomyocytes carrying a KCNH2 c.G1681A mutation in a IKr ion-channel pore, which caused impaired glycosylation and channel transport to cell surface. Allele-specific RNA interference (RNAi) directed towards the mutated KCNH2 mRNA caused knockdown, while leaving the wild-type mRNA unaffected. Electrophysiological analysis of patient-derived LQT2 hiPSC cardiomyocytes treated with mutation-specific siRNAs showed normalized action potential durations (APDs) and K+ currents with the concurrent rescue of spontaneous and drug-induced arrhythmias (presented as early-afterdepolarizations). Conclusions These findings provide in vitro evidence that allele-specific RNAi can rescue diseased phenotype in LQTS cardiomyocytes. This is a potentially novel route for the treatment of many autosomal-dominant-negative disorders, including those of the heart.
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spelling nottingham-26642020-05-04T16:36:07Z https://eprints.nottingham.ac.uk/2664/ Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes Matsa, Elena Dixon, James E. Medway, Christopher Georgiou, Orestis Patel, Minal J. Morgan, Kevin Kemp, Paul J. Staniforth, Andrew Mellor, Ian Denning, Chris Aims Long-QT syndromes (LQTS) are mostly autosomal-dominant congenital disorders associated with a 1:1000 mutation frequency, cardiac arrest, and sudden death. We sought to use cardiomyocytes derived from human-induced pluripotency stem cells (hiPSCs) as an in vitro model to develop and evaluate gene-based therapeutics for the treatment of LQTS. Methods and results We produced LQTS-type 2 (LQT2) hiPSC cardiomyocytes carrying a KCNH2 c.G1681A mutation in a IKr ion-channel pore, which caused impaired glycosylation and channel transport to cell surface. Allele-specific RNA interference (RNAi) directed towards the mutated KCNH2 mRNA caused knockdown, while leaving the wild-type mRNA unaffected. Electrophysiological analysis of patient-derived LQT2 hiPSC cardiomyocytes treated with mutation-specific siRNAs showed normalized action potential durations (APDs) and K+ currents with the concurrent rescue of spontaneous and drug-induced arrhythmias (presented as early-afterdepolarizations). Conclusions These findings provide in vitro evidence that allele-specific RNAi can rescue diseased phenotype in LQTS cardiomyocytes. This is a potentially novel route for the treatment of many autosomal-dominant-negative disorders, including those of the heart. Oxford University Press 2013-03-06 Article PeerReviewed Matsa, Elena, Dixon, James E., Medway, Christopher, Georgiou, Orestis, Patel, Minal J., Morgan, Kevin, Kemp, Paul J., Staniforth, Andrew, Mellor, Ian and Denning, Chris (2013) Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes. European Heart Journal . ISSN 0195-668X iPS cells Long-QT syndrome Arrhythmia Electrophysiology Gene therapy http://eurheartj.oxfordjournals.org/content/early/2013/03/06/eurheartj.eht067.full doi:10.1093/eurheartj/eht067 doi:10.1093/eurheartj/eht067
spellingShingle iPS cells
Long-QT syndrome
Arrhythmia
Electrophysiology
Gene therapy
Matsa, Elena
Dixon, James E.
Medway, Christopher
Georgiou, Orestis
Patel, Minal J.
Morgan, Kevin
Kemp, Paul J.
Staniforth, Andrew
Mellor, Ian
Denning, Chris
Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
title Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
title_full Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
title_fullStr Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
title_full_unstemmed Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
title_short Allele-specific RNA interference rescues the long-QT syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
title_sort allele-specific rna interference rescues the long-qt syndrome phenotype in human-induced pluripotency stem cell cardiomyocytes
topic iPS cells
Long-QT syndrome
Arrhythmia
Electrophysiology
Gene therapy
url https://eprints.nottingham.ac.uk/2664/
https://eprints.nottingham.ac.uk/2664/
https://eprints.nottingham.ac.uk/2664/