About: CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis

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About: CD36 overexpression predisposes to arrhythmias but reduces infarct size in spontaneously hypertensive rats: gene expression profile analysis Goto Sponge NotDistinct Permalink

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rdf:type	skos:Concept http://linked.opendata.cz/ontology/domain/vavai/Vysledek
rdfs:seeAlso	http://physiolgenomics.physiology.org/content/44/2/173.long
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. (en)
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 (en)
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 (en)
skos:notation	RIV/00216208:11310/12:10105668!RIV13-GA0-11310___
http://linked.open...avai/riv/aktivita	P S Z
http://linked.open...avai/riv/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)
http://linked.open...iv/cisloPeriodika	2
http://linked.open...vai/riv/dodaniDat	2013
http://linked.open...aciTvurceVysledku	Novák, František Klevstig, Martina Jiřina
http://linked.open.../riv/druhVysledku	J - Článek v odborném periodiku
http://linked.open...iv/duvernostUdaju	S - Úplné a pravdivé údaje nepodléhající ochraně podle zvláštních právních předpisů
http://linked.open...titaPredkladatele	Univerzita Karlova v Praze / Přírodovědecká fakulta
http://linked.open...dnocenehoVysledku	126167
http://linked.open...ai/riv/idVysledku	RIV/00216208:11310/12:10105668
http://linked.open...riv/jazykVysledku	eng - angličtina
http://linked.open.../riv/klicovaSlova	gene 54 expression profiles; infarct size; arrhythmias; spontaneously hypertensive rat; CD36 (en)
http://linked.open.../riv/klicoveSlovo	spontaneously hypertensive rat CD36 gene 54 expression profiles infarct size arrhythmias
http://linked.open...odStatuVydavatele	US - Spojené státy americké
http://linked.open...ontrolniKodProRIV	[9C69448A59AD]
http://linked.open...i/riv/nazevZdroje	Physiological Genomics
http://linked.open...in/vavai/riv/obor	FA
http://linked.open...ichTvurcuVysledku	2 (xsd:int)
http://linked.open...cetTvurcuVysledku	18 (xsd:int)
http://linked.open...vavai/riv/projekt	The use of ultrasound in nanomedicine Physiology of animal cell (2) The role of adrenergic signaling and oxidative stress in molecular mechanisms of cardioprotection induced by chronic hypoxia The mitochondrial genome and oxidative phosphorylation system in metabolic syndrome The effect of ectopic fat accumulation and chronic inflammation on the development of liver injury and disorders associated with insulin resistance. European large-scale functional genomics in the rat for translational research The role of Plzf (Promyelocytic leukemia zinc finger) gene in the pathogenesis of cardiovascular and metabolic disturbances in rat models Pathophysiology and genetics of metabolic syndrome in experimental models and humans The role of adipocytokines and fatty acids in the disorders of insulin sensitivity and insulin secretion in metabolic syndrome Center for Applied Genomics Centre for cardiovascular research Analysis of mechanisms of adipokine autocrine effects on glucose and lipid metabolism Genetic and correlation analyses of ectopic fat accumulation and adipose tissue oxidative/inflammatory processes and their role in the pathogenesis of insulin resistance The role of C reactive protein in the pathogenesis of metabolic syndrome: nutritional and pharmacological interventions
http://linked.open...UplatneniVysledku	2012
http://linked.open...v/svazekPeriodika	44
http://linked.open...iv/tvurceVysledku	Landa, Vladimír Mlejnek, Petr Neckář, Jan Novák, František Pravenec, Michal Seidman, J. G. Vecka, Marek Zídek, Václav Šimáková, Miroslava Kolář, František Drahota, Zdeněk Houštěk, Josef Šilhavý, Jan Papoušek, František Kazdová, Ludmila Klevstig, Martina Jiřina Kurtz, Theodore W. Siedman, Christine
http://linked.open...ain/vavai/riv/wos	000300048700007
http://linked.open...n/vavai/riv/zamer	Výzkum molekulárních a buněčných základů fyziologických a patofyziologických procesů s cílem objasnit mechanismy vzniku závažných onemocnění člověka Signaling and cellular response mechanisms Výzkum kardiovaskulárních nemocí, diabetu a transplantace životně důležitých orgánů
issn	1094-8341
number of pages	10 (xsd:int)
http://bibframe.org/vocab/doi	10.1152/physiolgenomics.00083.2011
http://localhost/t...ganizacniJednotka	11310

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