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Statements

Subject Item
n2:RIV%2F00216208%3A11310%2F12%3A10105668%21RIV13-GA0-11310___
rdf:type
n11:Vysledek skos:Concept
rdfs:seeAlso
http://physiolgenomics.physiology.org/content/44/2/173.long
dcterms:description
CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long-chain fatty acids (FA). Previously, we found that the spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene that results in reduced transport of long-chain FA into cardiomyocytes and predisposes the SHR to cardiac hypertrophy. In the current study, we analyzed the effects of mutant Cd36 on susceptibility to ischemic ventricular arrhythmias and myocardial infarction in adult SHR-Cd36 transgenic rats with wild type Cd36 compared to age-matched SHR controls. Using an open-chest model of coronary artery occlusion, we found that SHR-Cd36 transgenic rats showed profound arrhythmogenesis resulting in significantly increased duration of tachyarrhythmias (207+-48s vs. 55+-21s, P is lower then 0.05), total number of premature ventricular complexes (2623+-517 vs. 849+-250, P is lower then 0.05) and arrhythmia score (3.86+-0.18 vs. 3.13+-0.13, P is lower then 0.001). On the other hand, transgenic SHR compared to SHR controls showed significantly reduced infarct size (52.6+-4.3% vs. 72.4+-2.9% of area at risk, P is lower then 0.001). Similar differences were observed in isolated perfused hearts and the increased susceptibility of transgenic SHR to arrhythmias was abolished by reserpine suggesting the involvement of catecholamines. To further search for possible molecular mechanisms of altered ischemic tolerance, we compared gene expression profiles in left ventricles dissected from 6-week-old transgenic SHR versus age-matched controls using Illumina-based sequencing. Circadian rhythms and oxidative phosphorylation were identified as the top Kegg pathways while circadian rhythms, VDR/RXR activation, IGF1 signaling and HMGB1 signaling were the top IPA canonical pathways potentially important for Cd36-mediated effects on ischemic tolerance. CD36 fatty acid translocase plays a key role in supplying heart with its major energy substrate, long-chain fatty acids (FA). Previously, we found that the spontaneously hypertensive rat (SHR) harbors a deletion variant of Cd36 gene that results in reduced transport of long-chain FA into cardiomyocytes and predisposes the SHR to cardiac hypertrophy. In the current study, we analyzed the effects of mutant Cd36 on susceptibility to ischemic ventricular arrhythmias and myocardial infarction in adult SHR-Cd36 transgenic rats with wild type Cd36 compared to age-matched SHR controls. Using an open-chest model of coronary artery occlusion, we found that SHR-Cd36 transgenic rats showed profound arrhythmogenesis resulting in significantly increased duration of tachyarrhythmias (207+-48s vs. 55+-21s, P is lower then 0.05), total number of premature ventricular complexes (2623+-517 vs. 849+-250, P is lower then 0.05) and arrhythmia score (3.86+-0.18 vs. 3.13+-0.13, P is lower then 0.001). On the other hand, transgenic SHR compared to SHR controls showed significantly reduced infarct size (52.6+-4.3% vs. 72.4+-2.9% of area at risk, P is lower then 0.001). Similar differences were observed in isolated perfused hearts and the increased susceptibility of transgenic SHR to arrhythmias was abolished by reserpine suggesting the involvement of catecholamines. To further search for possible molecular mechanisms of altered ischemic tolerance, we compared gene expression profiles in left ventricles dissected from 6-week-old transgenic SHR versus age-matched controls using Illumina-based sequencing. Circadian rhythms and oxidative phosphorylation were identified as the top Kegg pathways while circadian rhythms, VDR/RXR activation, IGF1 signaling and HMGB1 signaling were the top IPA canonical pathways potentially important for Cd36-mediated effects on ischemic tolerance.
dcterms:title
CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis
skos:prefLabel
CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis
skos:notation
RIV/00216208:11310/12:10105668!RIV13-GA0-11310___
n11:predkladatel
n19:orjk%3A11310
n3:aktivita
n6:Z n6:S n6:P
n3:aktivity
P(1M0510), P(1M0520), P(7E10067), P(GAP301/10/0756), P(GD305/08/H037), P(IAA500110805), P(IAAX01110901), P(KAN200520703), P(ME08006), P(NR9359), P(NR9387), P(NS10504), P(NS9757), P(OC08017), S, Z(AV0Z50110509), Z(MSM0021620858), Z(MZ0IKEM2005)
n3:cisloPeriodika
2
n3:dodaniDat
n4:2013
n3:domaciTvurceVysledku
n16:9895957 n16:8079404
n3:druhVysledku
n10:J
n3:duvernostUdaju
n20:S
n3:entitaPredkladatele
n22:predkladatel
n3:idSjednocenehoVysledku
126167
n3:idVysledku
RIV/00216208:11310/12:10105668
n3:jazykVysledku
n17:eng
n3:klicovaSlova
gene 54 expression profiles; infarct size; arrhythmias; spontaneously hypertensive rat; CD36
n3:klicoveSlovo
n8:CD36 n8:infarct%20size n8:arrhythmias n8:gene%2054%20expression%20profiles n8:spontaneously%20hypertensive%20rat
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[9C69448A59AD]
n3:nazevZdroje
Physiological Genomics
n3:obor
n21:FA
n3:pocetDomacichTvurcuVysledku
2
n3:pocetTvurcuVysledku
18
n3:projekt
n5:1M0510 n5:OC08017 n5:GAP301%2F10%2F0756 n5:NR9359 n5:NR9387 n5:IAAX01110901 n5:7E10067 n5:KAN200520703 n5:GD305%2F08%2FH037 n5:1M0520 n5:ME08006 n5:NS10504 n5:IAA500110805 n5:NS9757
n3:rokUplatneniVysledku
n4:2012
n3:svazekPeriodika
44
n3:tvurceVysledku
Vecka, Marek Kolář, František Kurtz, Theodore W. Zídek, Václav Kazdová, Ludmila Šilhavý, Jan Pravenec, Michal Klevstig, Martina Jiřina Siedman, Christine Seidman, J. G. Novák, František Neckář, Jan Drahota, Zdeněk Houštěk, Josef Mlejnek, Petr Šimáková, Miroslava Papoušek, František Landa, Vladimír
n3:wos
000300048700007
n3:zamer
n9:MSM0021620858 n9:MZ0IKEM2005 n9:AV0Z50110509
s:issn
1094-8341
s:numberOfPages
10
n14:doi
10.1152/physiolgenomics.00083.2011
n7:organizacniJednotka
11310