scholarly journals Network construction of aberrantly expressed miRNAs and their target mRNAs in ventricular myocardium with ischemia–reperfusion arrhythmias

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Jian Tang ◽  
Hong Gao ◽  
Yanqiu Liu ◽  
Jing Song ◽  
Yurong Feng ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Ventricular Myocardium ◽  
Reperfusion Arrhythmias ◽  
Network Construction ◽  
Target Mrnas

scholarly journals Network construction of aberrantly expressed miRNAs and their target mRNAs in ventricular myocardium with ischemia–reperfusion arrhythmias

2019 ◽  
Author(s):  
Jian Tang ◽  
Hong Gao ◽  
Yanqiu Liu ◽  
Jing Song ◽  
Yurong Feng ◽  
...  
Keyword(s):  
High Throughput Sequencing ◽  
Target Genes ◽  
Expression Profiles ◽  
Ischemia Reperfusion ◽  
Interaction Network ◽  
Ventricular Myocardium ◽  
Functional Study ◽  
Network Graph ◽  
Reperfusion Arrhythmias ◽  
Mrna Targets

Abstract Background: Increasing evidences have verified that microRNAs (miRNAs) play an important role in formation and progression of various cardiac diseases including arrhythmias. Existing research has showed that certain miRNAs exhibit significantly different expressions and effects in arrhythmias. However, the effect of miRNAs in the progression of hypothermic ischemic–reperfusion arrhythmias (RA) and its potential mechanism remains to be further discussed. Methods: By utilizing a model for hypothermic ischemia–reperfusion of rats, miRNAs expression profiles of ventricular myocardium with global hypothermic ischemia–reperfusion and those of ventricular myocardium with hypothermic ischemia–RA were established through high-throughput sequencing. Furthermore, the aberrantly expressed miRNAs in myocardium with and without hypothermic ischemia–RA were screened and verified. By applying RNAhybrid, MiRanda, and TargetScan software, the target genes of these aberrantly expressed miRNAs were predicted. Based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, the mRNA targets associated with these miRNAs were determined and the miRNA–mRNA interaction during the progression of cardiovascular diseases was explored. The aberrantly expressed miRNAs related to hypothermic ischemia–RA were validated by employing quantitative fluorescence polymerase chain reaction (PCR). Results: Eight significantly aberrantly expressed miRNAs were identified(novel-miR-1 、novel-miR-16、novel-miR-17、novel-miR-19、novel-miR-30、novel-miR-43、rno-miR-122-5p、rno-miR-429), in which six were up-regulated and two were down-regulated. Moreover, target genes and signaling pathways associated with these aberrantly expressed miRNAs were predicted and analyzed. According to miRNA–mRNA interaction network graph, it was revealed that GJA1 gene was considered as the target of novel-miR-17. Conclusions: Aberrantly expressed miRNAs were possibly associated with the formation mechanism of hypothermic ischemia–RA. Specific miRNAs, such as novel-miR-17 and rno-miR-429 are probably new potential targets for further conducting functional study on hypothermic ischemia–RA.

scholarly journals Cardioprotective Effects of Quercetin Against Ischemia-Reperfusion Injury Are Age-Dependent

2016 ◽  
pp. S101-S107 ◽  
Author(s):  
M. BARTEKOVA ◽  
J. RADOSINSKA ◽  
D. PANCZA ◽  
M. BARANCIK ◽  
T. RAVINGEROVA
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reperfusion Arrhythmias ◽  
Beneficial Effects ◽  
Adult Rat ◽  
Rat Hearts ◽  
Age Dependent ◽  
Old Rats ◽  
Contraction And Relaxation ◽  
Quercetin Treatment

Quercetin, a polyphenolic compound present in various types of food, has been shown to exert beneficial effects in different cardiac as well as non-cardiac ischemia/reperfusion (I/R) models in adult animals. However, there is no evidence about the effects of quercetin on I/R injury in non-mature animals, despite the fact that efficiency of some interventions against I/R is age-dependent. This study was aimed to investigate the effects of chronic quercetin treatment on I/R injury in juvenile and adult rat hearts. Juvenile (4-week-old) as well as adult (12-week-old) rats were treated with quercetin (20 mg/kg/day) for 4 weeks, hearts were excised and exposed to 25-min global ischemia followed by 40-min reperfusion. Functional parameters of hearts and occurrence of reperfusion arrhythmias were registered to assess the cardiac function. Our results have shown that quercetin improved post-ischemic recovery of LVDP, as well as recovery of markers of contraction and relaxation, +(dP/dt)max and –(dP/dt)max, respectively, in juvenile hearts, but not in adult hearts. Quercetin had no impact on incidence as well as duration of reperfusion arrhythmias in animals of both ages. We conclude that the age of rats plays an important role in heart response to quercetin treatment in the particular dose and duration of the treatment. Therefore, the age of the treated subjects should be taken into consideration when choosing the dose of quercetin and duration of its application in prevention and/or treatment of cardiovascular diseases.

17β-Estradiol Prevents Dysfunction of Canine Coronary Endothelium and Myocardium and Reperfusion Arrhythmias After Brief Ischemia/Reperfusion

Circulation ◽  
1996 ◽  
Vol 94 (11) ◽  
pp. 2901-2908 ◽  
Author(s):  
Young D. Kim ◽  
Barbara Chen ◽  
John Beauregard ◽  
Peter Kouretas ◽  
George Thomas ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Reperfusion Arrhythmias ◽  
17Β Estradiol ◽  
Coronary Endothelium

scholarly journals Effects of Na+/H+ exchange inhibition on myocardial ischemia/reperfusion arrhythmias

1999 ◽  
Vol 79 ◽  
pp. 23
Author(s):  
Keitaro Hashimoto ◽  
Atsushi Sugiyama ◽  
Nu Nu Aye ◽  
Chikaomi Yamada ◽  
Daisuke Chino
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Reperfusion Arrhythmias ◽  
Myocardial Ischemia Reperfusion

Antioxidant tempol suppresses heart cytosolic phospholipase A2α stimulated by chronic intermittent hypoxia

2017 ◽  
Vol 95 (8) ◽  
pp. 920-927 ◽  
Author(s):  
Petra Míčová ◽  
Martina Klevstig ◽  
Kristýna Holzerová ◽  
Marek Vecka ◽  
Jitka Žurmanová ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Chronic Intermittent Hypoxia ◽  
Acute Ischemia ◽  
Left Ventricular Myocardium ◽  
Ros Generation ◽  
Mrna Levels

Adaptation to chronic intermittent hypoxia (CIH) is associated with reactive oxygen species (ROS) generation implicated in the improved cardiac tolerance against acute ischemia–reperfusion injury. Phospholipases A2(PLA2s) play an important role in cardiomyocyte phospholipid metabolism influencing membrane homeostasis. Here we aimed to determine the effect of CIH (7000 m, 8 h/day, 5 weeks) on the expression of cytosolic PLA2(cPLA2α), its phosphorylated form (p-cPLA2α), calcium-independent (iPLA2), and secretory (sPLA2IIA) at protein and mRNA levels, as well as fatty acids (FA) profile in left ventricular myocardium of adult male Wistar rats. Chronic administration of antioxidant tempol was used to verify the ROS involvement in CIH effect on PLA2s expression and phospholipid FA remodeling. While CIH did not affect PLA2s mRNA levels, it increased the total cPLA2α protein in cytosol and membranes (by 191% and 38%, respectively) and p-cPLA2α (by 23%) in membranes. On the contrary, both iPLA2and sPLA2IIA were downregulated by CIH. CIH further decreased phospholipid n-6 polyunsaturated FA (PUFA) and increased n-3 PUFA proportion. Tempol treatment prevented only CIH-induced cPLA2α up-regulation and its phosphorylation on Ser505. Our results show that CIH diversely affect myocardial PLA2s and suggest that ROS are responsible for the activation of cPLA2α under these conditions.

Abstract 11685: Early Myocardial Gene Expression Profiling After Deep Hypothermic Circulatory Arrest Reveals Ontogenetic Adaptive Mechanisms Underlying Ischemia-Reperfusion Tolerance in the Swine

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Miki Yamada ◽  
Amir Sheikh ◽  
Kevin Collins ◽  
James Frederiksen ◽  
George Quick ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Troponin I ◽  
Ischemia Reperfusion ◽  
Circulatory Arrest ◽  
Expression Patterns ◽  
Ventricular Myocardium ◽  
Deep Hypothermic Circulatory Arrest ◽  
Left Ventricular ◽  
Hypothermic Circulatory Arrest ◽  
Left Ventricular Myocardium

Previous studies suggest that immature hearts are more tolerant to ischemia than adult myocardium; whether differences exist during ontogenic development in severity of global myocardial ischemia/reperfusion (I/R) injury associated with cardiac surgery remains unknown. We employed swine models of deep hypothermic circulatory arrest (DHCA) to test the hypothesis that early differential regulation of cardioprotective genes is associated with increased tolerance of neonatal myocardium to surgical I/R. Male neonatal and adult pigs were randomized to DHCA or sham (N=5-14/group). DHCA animals underwent cardiopulmonary bypass (18°C), DHCA 60 min, and were recovered for 3h. Severity of perioperative myocardial injury was determined biochemically (Troponin I) and echocardiographically. Transcript levels were quantified in left ventricular myocardium using Affymetrix Porcine Genome arrays, followed by differential expression and pathway analysis. A 2-fold increase in severity of perioperative myocardial injury was found in adult pigs (Fig.A). Of 596 transcripts differentially expressed in neonates (≥1.5-fold change, DHCA vs. sham, FDR<0.05), 53 were shared with adults (Fig.B). Among them, divergent expression patterns were found for oxysterol binding protein-like 6 (down-regulated in adults up-regulated in neonates) and bromodomain adjacent to zinc finger domain 2B (up-regulated in adults - down-regulated in neonates). Top transcripts uniquely upregulated in neonates but unchanged in adults were the apoptosis inhibitor baculoviral IAP repeat containing 2, and signal transducer and activator of transcription 3. mTOR signaling and p53 signaling were the top canonical pathways deregulated in adults and neonates, respectively. A high resistance to surgical I/R injury in neonatal vs adult swine heart is correlated with robust differences in early transcriptional programs, suggesting the involvement of fundamental adaptive ontogenetic processes.

Ischemia-reperfusion arrhythmias and lipids: Effect of human high- and low-density lipoproteins on reperfusion arrhythmias

1991 ◽  
Vol 5 (S2) ◽  
pp. 269-276 ◽  
Author(s):  
Seibu Mochizuki ◽  
Mitsuru Okumura ◽  
Fumio Tanaka ◽  
Takeshi Sato ◽  
Akihiko Kagami ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Reperfusion Arrhythmias

Ins(1,4,5)P3 and arrhythmogenic responses during myocardial reperfusion: evidence for receptor specificity

1997 ◽  
Vol 273 (3) ◽  
pp. H1119-H1125 ◽  
Author(s):  
A. N. Jacobsen ◽  
X. J. Du ◽  
A. M. Dart ◽  
E. A. Woodcock
Keyword(s):  
Ventricular Fibrillation ◽  
G Proteins ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Ischemia Reperfusion ◽  
Myocardial Reperfusion ◽  
Reperfusion Arrhythmias ◽  
Rat Hearts ◽  
Inositol 1,4,5 Trisphosphate ◽  
Phosphate Response

Reperfusion of ischemic rat hearts initiates the generation of inositol(1,4,5)trisphosphate [Ins(1,4,5)P3] and arrhythmias, provided that either norepinephrine or thrombin is present. In the current study, effects on endothelin-1 (ET-1) responses were investigated. Reperfusion of catecholamine-depleted, [3H]inositol-labeled hearts in the presence of ET-1 caused an increase in [3H]inositol phosphates (7,073 +/- 1,004 to 17,300 +/- 206 counts.min-1.g tissue-1, means +/- SE, n = 4, P < 0.01), which was quantitatively greater than the release observed under normoxic conditions, but there was no increase in [3H]Ins(1,4,5)P3. Gentamicin (150 microM) inhibited inositol phosphate responses in the presence of either norepinephrine or thrombin but did not inhibit the response to ET-1, providing additional evidence that the inositol phosphate response to ET-1 does not involve formation of Ins(1,4,5)P3, even under reperfusion conditions. In contrast to norepinephrine and thrombin, ET-1 did not initiate reperfusion arrhythmias (4.4% ventricular fibrillation compared with 0% ventricular fibrillation in catecholamine-depleted controls). The data provide strong evidence that the effect of ischemia-reperfusion on inositol phosphate responses is specific for particular receptor types and eliminates G proteins, phospholipase C enzymes, and substrate availability as the primary factors responsible for Ins(1,4,5)P3 generation under reperfusion conditions.

Chronic skeletal muscle ischemia preserves coronary flow in the ischemic rat heart

2011 ◽  
Vol 301 (4) ◽  
pp. H1229-H1235 ◽  
Author(s):  
Varnavas C. Varnavas ◽  
Konstantinos Kontaras ◽  
Chryssoula Glava ◽  
Christos D. Maniotis ◽  
Michael Koutouzis ◽  
...  
Keyword(s):  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Coronary Flow ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Hindlimb Ischemia ◽  
Muscle Ischemia

Chronic skeletal muscle ischemia confers cytoprotection to the ventricular myocardium during infarction, but the underlying mechanisms remain unclear. Although neovascularization in the left ventricular myocardium has been proposed as a possible mechanism, the functional capacity of such vessels has not been studied. We examined the effects of chronic limb ischemia on infarct size, coronary blood flow, and left ventricular function after ischemia-reperfusion. Hindlimb ischemia was induced in 65 Wistar rats by excision of the left femoral artery, whereas 65 rats were sham operated. After 4 wk, myocardial infarction was generated by permanent coronary artery ligation. Infarct size was measured 24 h postligation. Left ventricular function was evaluated in isolated hearts after ischemia-reperfusion, 4 wk after limb ischemia. Neovascularization was assessed by immunohistochemistry, and coronary flow was measured under maximum vasodilatation at different perfusion pressures before and after coronary ligation. Infarct size was smaller after limb ischemia compared with controls (24.4 ± 8.1% vs. 46.2 ± 9.5% of the ventricle and 47.6 ± 8.7% vs. 80.1 ± 9.3% of the ischemic area, respectively). Indexes of left ventricular function at the end of reperfusion (divided by baseline values) were improved after limb ischemia (developed pressure: 0.68 ± 0.06 vs. 0.59 ± 0.05, P = 0.008; maximum +dP/d t: 0.70 ± 0.08 vs. 0.59 ± 0.04, P = 0.004; and maximum −dP/d t: 0.86 ± 0.14 vs. 0.72 ± 0.10, P = 0.041). Coronary vessel density was markedly higher ( P = 0.00021) in limb ischemic rats. In contrast to controls ( F = 5.65, P = 0.00182), where coronary flow decreased, it remained unchanged ( F = 1.36, P = 0.28) after ligation in limb ischemic rats. In conclusion, chronic hindlimb ischemia decreases infarct size and attenuates left ventricular dysfunction by increasing coronary collateral vessel density and blood flow.

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