Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death

Abstract Background Long QT Syndrome Type-2 (LQT2) is due to loss-of-function KCNH2 variants. KCNH2 encodes Kv11.1 that forms a delayed-rectifier potassium channel in the brain and heart. LQT2 is associated with arrhythmias, seizures, sudden cardiac death, and sudden unexpected death in epilepsy (SU...

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Main Authors: Veronica Singh, Kyle T. Wagner, Laura G. Williams, Justin M. Ryan, Katherine R. Keller, Jonathan D. Mohnkern, Robert S. Gardner, Louis T. Dang, Julie M. Ziobro, Richard J. H. Wojcikiewicz, Nathan R. Tucker, David S. Auerbach
Format: Article
Language:English
Published: BMC 2025-04-01
Series:Journal of Translational Medicine
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Online Access:https://doi.org/10.1186/s12967-025-06382-w
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author Veronica Singh
Kyle T. Wagner
Laura G. Williams
Justin M. Ryan
Katherine R. Keller
Jonathan D. Mohnkern
Robert S. Gardner
Louis T. Dang
Julie M. Ziobro
Richard J. H. Wojcikiewicz
Nathan R. Tucker
David S. Auerbach
author_facet Veronica Singh
Kyle T. Wagner
Laura G. Williams
Justin M. Ryan
Katherine R. Keller
Jonathan D. Mohnkern
Robert S. Gardner
Louis T. Dang
Julie M. Ziobro
Richard J. H. Wojcikiewicz
Nathan R. Tucker
David S. Auerbach
author_sort Veronica Singh
collection DOAJ
description Abstract Background Long QT Syndrome Type-2 (LQT2) is due to loss-of-function KCNH2 variants. KCNH2 encodes Kv11.1 that forms a delayed-rectifier potassium channel in the brain and heart. LQT2 is associated with arrhythmias, seizures, sudden cardiac death, and sudden unexpected death in epilepsy (SUDEP). The goal of the study is to develop a translational model that reproduces the neuro-cardiac electrical abnormalities and sudden death seen in people with LQT2. Methods We generated the first knock-in rabbit model of LQT2 (Kcnh2 (+/7bp−del)), due to a 7 base-pair (7bp) deletion in the pore domain of the endogenous rabbit Kcnh2 gene. Results Mutant Kcnh2 is expressed in the heart and brain and constitutes 11% of total Kcnh2 in Kcnh2 (+/7bp−del) rabbits. Total Kcnh2, WT Kcnh2, and WT Kv11.1 expression is lower in Kcnh2 (+/7bp−del) vs. WT rabbits. Kcnh2 (+/7bp−del) rabbits exhibit prolonged cardiac ventricular repolarization (QTc, JTec, JTpc). There is an increased prevalence of spontaneous epileptiform activity and clinical seizures in Kcnh2 (+/7bp−del) (7 of 37 rabbits) vs. WT rabbits (1:68 rabbits, p < 0.003). 18.9% of Kcnh2 (+/7bp−del) vs. 1.5% of WT rabbits died suddenly and spontaneously (p < 0.003). We recorded 2 spontaneous lethal events in Kcnh2 (+/7bp−del) rabbits: (1) sudden cardiac death and (2) seizure-mediated sudden death due to generalized tonic-clonic seizures, post-ictal generalized EEG suppression, bradycardia, ECG-T-wave inversion, focal cardiac activity, and asystole/death. Conclusions We developed the first genetic rabbit model of LQT2 that reproduces the cardiac and epileptic phenotypes seen in people with LQT2. Kcnh2 (+/7bp−del) rabbits provide a valuable tool for future mechanistic studies, development of neurotherapeutics, and cardiac-safety testing.
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spelling doaj-art-11946963346d45ebaff028358decf7e22025-08-20T02:17:49ZengBMCJournal of Translational Medicine1479-58762025-04-0123111510.1186/s12967-025-06382-wKnock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden deathVeronica Singh0Kyle T. Wagner1Laura G. Williams2Justin M. Ryan3Katherine R. Keller4Jonathan D. Mohnkern5Robert S. Gardner6Louis T. Dang7Julie M. Ziobro8Richard J. H. Wojcikiewicz9Nathan R. Tucker10David S. Auerbach11Department of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pediatrics, University of MichiganDepartment of Pediatrics, University of MichiganDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityDepartment of Pharmacology, SUNY Upstate Medical UniversityAbstract Background Long QT Syndrome Type-2 (LQT2) is due to loss-of-function KCNH2 variants. KCNH2 encodes Kv11.1 that forms a delayed-rectifier potassium channel in the brain and heart. LQT2 is associated with arrhythmias, seizures, sudden cardiac death, and sudden unexpected death in epilepsy (SUDEP). The goal of the study is to develop a translational model that reproduces the neuro-cardiac electrical abnormalities and sudden death seen in people with LQT2. Methods We generated the first knock-in rabbit model of LQT2 (Kcnh2 (+/7bp−del)), due to a 7 base-pair (7bp) deletion in the pore domain of the endogenous rabbit Kcnh2 gene. Results Mutant Kcnh2 is expressed in the heart and brain and constitutes 11% of total Kcnh2 in Kcnh2 (+/7bp−del) rabbits. Total Kcnh2, WT Kcnh2, and WT Kv11.1 expression is lower in Kcnh2 (+/7bp−del) vs. WT rabbits. Kcnh2 (+/7bp−del) rabbits exhibit prolonged cardiac ventricular repolarization (QTc, JTec, JTpc). There is an increased prevalence of spontaneous epileptiform activity and clinical seizures in Kcnh2 (+/7bp−del) (7 of 37 rabbits) vs. WT rabbits (1:68 rabbits, p < 0.003). 18.9% of Kcnh2 (+/7bp−del) vs. 1.5% of WT rabbits died suddenly and spontaneously (p < 0.003). We recorded 2 spontaneous lethal events in Kcnh2 (+/7bp−del) rabbits: (1) sudden cardiac death and (2) seizure-mediated sudden death due to generalized tonic-clonic seizures, post-ictal generalized EEG suppression, bradycardia, ECG-T-wave inversion, focal cardiac activity, and asystole/death. Conclusions We developed the first genetic rabbit model of LQT2 that reproduces the cardiac and epileptic phenotypes seen in people with LQT2. Kcnh2 (+/7bp−del) rabbits provide a valuable tool for future mechanistic studies, development of neurotherapeutics, and cardiac-safety testing.https://doi.org/10.1186/s12967-025-06382-wArrhythmiaSeizureEpilepsyLong QT syndromeRabbitKCNH2
spellingShingle Veronica Singh
Kyle T. Wagner
Laura G. Williams
Justin M. Ryan
Katherine R. Keller
Jonathan D. Mohnkern
Robert S. Gardner
Louis T. Dang
Julie M. Ziobro
Richard J. H. Wojcikiewicz
Nathan R. Tucker
David S. Auerbach
Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death
Journal of Translational Medicine
Arrhythmia
Seizure
Epilepsy
Long QT syndrome
Rabbit
KCNH2
title Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death
title_full Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death
title_fullStr Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death
title_full_unstemmed Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death
title_short Knock-in Kcnh2 rabbit model of long QT syndrome type-2, epilepsy, and sudden death
title_sort knock in kcnh2 rabbit model of long qt syndrome type 2 epilepsy and sudden death
topic Arrhythmia
Seizure
Epilepsy
Long QT syndrome
Rabbit
KCNH2
url https://doi.org/10.1186/s12967-025-06382-w
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