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Statements

Subject Item
n2:RIV%2F00216208%3A11110%2F13%3A10174160%21RIV14-GA0-11110___
rdf:type
n9:Vysledek skos:Concept
rdfs:seeAlso
http://dx.doi.org/10.1093/cvr/cvt076
dcterms:description
Aims Ion channel remodelling and ventricular conduction system (VCS) alterations play relevant roles in the generation of cardiac arrhythmias, but the interaction between ion channel remodelling and cardiac conduction system dysfunctions in an arrhythmogenic context remain unexplored. Methods and results We have used a transgenic mouse line previously characterized as an animal model of Long QT Syndrome (LQTS) to analyse ion channel remodelling and VCS configuration. Reverse transcriptase-PCR and immunohistochemistry analysis showed early cardiac sodium channel upregulation at embryonic stages prior to the onset of Kv potassium channel remodelling, and cardiac hypertrophy at foetal stages. In line with these findings, patch-clamp assays demonstrated changes in sodium current density and a slowing of recovery from inactivation. Functional analysis by optical mapping revealed an immature ventricular activation pattern as well as an increase in the total left ventricle activation time in foetal transgenic hearts. Morphological analysis of LQTS transgenic mice in a Cx40(GFP/+) background demonstrated VCS dysmorphogenesis during heart development. Conclusions Our data demonstrate early sodium channel remodelling secondary to I-Ks blockage in a mouse model of LQTS leading to morphological and functional anomalies in the developing VCS and cardiac hypertrophy. These results provide new insights into the mechanisms underlying foetal and neonatal cardiac electrophysiological disorders, which might help understand how molecular, functional, and morphological alterations are linked to clinical pathologies such as cardiac congenital anomalies, arrhythmias, and perinatal sudden death. Aims Ion channel remodelling and ventricular conduction system (VCS) alterations play relevant roles in the generation of cardiac arrhythmias, but the interaction between ion channel remodelling and cardiac conduction system dysfunctions in an arrhythmogenic context remain unexplored. Methods and results We have used a transgenic mouse line previously characterized as an animal model of Long QT Syndrome (LQTS) to analyse ion channel remodelling and VCS configuration. Reverse transcriptase-PCR and immunohistochemistry analysis showed early cardiac sodium channel upregulation at embryonic stages prior to the onset of Kv potassium channel remodelling, and cardiac hypertrophy at foetal stages. In line with these findings, patch-clamp assays demonstrated changes in sodium current density and a slowing of recovery from inactivation. Functional analysis by optical mapping revealed an immature ventricular activation pattern as well as an increase in the total left ventricle activation time in foetal transgenic hearts. Morphological analysis of LQTS transgenic mice in a Cx40(GFP/+) background demonstrated VCS dysmorphogenesis during heart development. Conclusions Our data demonstrate early sodium channel remodelling secondary to I-Ks blockage in a mouse model of LQTS leading to morphological and functional anomalies in the developing VCS and cardiac hypertrophy. These results provide new insights into the mechanisms underlying foetal and neonatal cardiac electrophysiological disorders, which might help understand how molecular, functional, and morphological alterations are linked to clinical pathologies such as cardiac congenital anomalies, arrhythmias, and perinatal sudden death.
dcterms:title
Functional suppression of Kcnq1 leads to early sodium channel remodelling and cardiac conduction system dysmorphogenesis Functional suppression of Kcnq1 leads to early sodium channel remodelling and cardiac conduction system dysmorphogenesis
skos:prefLabel
Functional suppression of Kcnq1 leads to early sodium channel remodelling and cardiac conduction system dysmorphogenesis Functional suppression of Kcnq1 leads to early sodium channel remodelling and cardiac conduction system dysmorphogenesis
skos:notation
RIV/00216208:11110/13:10174160!RIV14-GA0-11110___
n9:predkladatel
n12:orjk%3A11110
n3:aktivita
n4:Z n4:P n4:I
n3:aktivity
I, P(GA13-12412S), P(GA304/08/0615), P(GAP302/11/1308), P(GD204/09/H084), Z(AV0Z50110509), Z(MSM0021620806)
n3:cisloPeriodika
3
n3:dodaniDat
n18:2014
n3:domaciTvurceVysledku
n21:5754623
n3:druhVysledku
n7:J
n3:duvernostUdaju
n22:S
n3:entitaPredkladatele
n17:predkladatel
n3:idSjednocenehoVysledku
75888
n3:idVysledku
RIV/00216208:11110/13:10174160
n3:jazykVysledku
n13:eng
n3:klicovaSlova
Cardiac hypertrophy; Sudden death; Long-QT syndrome; Ion channels
n3:klicoveSlovo
n14:Sudden%20death n14:Long-QT%20syndrome n14:Ion%20channels n14:Cardiac%20hypertrophy
n3:kodStatuVydavatele
NL - Nizozemsko
n3:kontrolniKodProRIV
[7DE27DCCF007]
n3:nazevZdroje
Cardiovascular Research
n3:obor
n10:FA
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
7
n3:projekt
n15:GA304%2F08%2F0615 n15:GA13-12412S n15:GD204%2F09%2FH084 n15:GAP302%2F11%2F1308
n3:rokUplatneniVysledku
n18:2013
n3:svazekPeriodika
98
n3:tvurceVysledku
Domínguez, Jorge N. Sedmera, David Aránega, Amelia E. de la Rosa, Angel J. Hove-Madsen, Leif Franco, Diego Šaňková, Barbora
n3:wos
000319428700021
n3:zamer
n6:AV0Z50110509 n6:MSM0021620806
s:issn
0008-6363
s:numberOfPages
11
n19:doi
10.1093/cvr/cvt076
n11:organizacniJednotka
11110