Soluble epoxide hydrolase inhibitors, t-AUCB, regulated microRNA-1 and its target genes in myocardial infarction mice

Gui, Yajun; Yang, Tao; Liu, Qiong; Liao, Caixiu; Chen, Jingyuan; Wang, Yating; Jiahui, HU; Xu, Danyan

doi:10.18632/oncotarget.21831

Cited by 16 publications

(24 citation statements)

References 37 publications

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“…MiR-1 is a muscle-specific miR reported to be tightly associated with CVD. Regarding I/R injury, miR-1 was found to be down-regulated in response to myocardial I/R injury in the heart tissue of rats [48,49] and mice [50], as well as in cardiac-derived H9c2 cells [48] and neonatal cardiac myocytes [51] exposed to hypoxia/reoxygenation (H/R). The level of miR-1 down-regulation was increased with prolonged time of MI in rats, and also with prolonged time of post-hypoxic reoxygenation in H9c2 cells [48].…”

Section: Role Of Mir-1 In Cardiac I/r Injurymentioning

confidence: 99%

“…↓miR-1 in heart tissue in response to I/R in rats, mice, and infarcted human hearts [48][49][50]52,53] ↓miR-1 in H9c2 cells and neonatal cardiac myocytes in response to H/R [48,51] ↑miR-1 in remote myocardium compared to infarcted zone or healthy hearts in infarcted human hearts [54] ↑levels of circulating miR-1 after AMI in pigs and humans [58,59] miR-1 overexpression exacerbated cardiac I/R injury in transgenic mice [55] miR-1 inhibition protects against I/R (H/R) injury in rats, mice, and H9c2 cells [48,55,56] miR-21…”

Section: Type Of Cvd Mir Findings Referencementioning

confidence: 99%

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Potential Clinical Implications of miR-1 and miR-21 in Heart Disease and Cardioprotection

Kura

Kaločayová

Devaux

et al. 2020

IJMS

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The interest in non-coding RNAs, which started more than a decade ago, has still not weakened. A wealth of experimental and clinical studies has suggested the potential of non-coding RNAs, especially the short-sized microRNAs (miRs), to be used as the new generation of therapeutic targets and biomarkers of cardiovascular disease, an ever-growing public health issue in the modern world. Among the hundreds of miRs characterized so far, microRNA-1 (miR-1) and microRNA-21 (miR-21) have received some attention and have been associated with cardiac injury and cardioprotection. In this review article, we summarize the current knowledge of the function of these two miRs in the heart, their association with cardiac injury, and their potential cardioprotective roles and biomarker value. While this field has already been extensively studied, much remains to be done before research findings can be translated into clinical application for patient’s benefit.

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Section: Role Of Mir-1 In Cardiac I/r Injurymentioning

confidence: 99%

Section: Type Of Cvd Mir Findings Referencementioning

confidence: 99%

Potential Clinical Implications of miR-1 and miR-21 in Heart Disease and Cardioprotection

Kura

Kaločayová

Devaux

et al. 2020

IJMS

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“…Abnormal upregulation of miR-1 suppresses the expression of genes related to the potassium voltage-gated channel subfamily J member 2/Inwardly rectifying K channel 2.1 and the gap junction protein alpha 1/connexin 43 pathway which may then induce arrhythmia by interfering with the K + current during repolarization (Gui et al, 2017).…”

Section: Arrhythmiamentioning

confidence: 99%

“…Currently, it is believed that myocardial ischemia can activate the β-adrenoceptor (βAR)/cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signal pathway, following activated PKA transfers to the nucleus and phosphorylates cAMPresponsive element binding protein CREB. Activated CREB promotes the transcription of miR-1 and other miRNAs (Gui et al, 2017;Shi and Yang, 2016).…”

Section: Myocardial Infarctionmentioning

confidence: 99%

Potential roles of microRNA-1 and microRNA-133 in cardiovascular disease

Song

Gao

Yan

2020

Rev. Cardiovasc. Med.

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Cardiovascular disease is still the main cause of morbidity and mortality worldwide. Currently, the frontier of research into cardiovascular disease is the field of noncoding RNA. In this review, information was collected on the use of micro-RNAs as non-invasive biomarkers and their role in pathophysiological processes and therapeutic applications. In the case of microRNA-1 and microRNA-133, the roles and regulatory mechanisms of them are reviewed for arrhythmia, myocardial infarction, diabetic cardiomyopathy, myocardial hypertrophy, cardiomyocyte differentiation, and cell reprogramming. It was observed that microRNA-1 and microRNA-133 do not exist independently, but are two co-transcriptional and cooperative regulatory factors. They have diagnostic value as biomarkers, but also have the potential as therapeutic targets such as for antiarrhythmia and cardiac reprogramming.

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“…Therefore, miR-133 could be a new target for treating ischemic arrhythmias. We previously demonstrated that sEHIs might reduce the incidence of ischemic arrhythmias by suppressing miR-1 in cardiomyocytes [ 18 , 19 ]. As miR-1 and miR-133 are clustered on the same chromosome loci and transcribed together in a tissue-specific manner [ 20 ], we speculated that miR-133 might also contribute to the anti-arrhythmic action of sEHIs.…”

Section: Introductionmentioning

confidence: 99%

Soluble epoxide hydrolase inhibitors, t-AUCB, downregulated miR-133 in a mouse model of myocardial infarction

Gui

Chen

et al. 2018

Lipids Health Dis

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BackgroundIt has been demonstrated that soluble epoxide hydrolase inhibitors (sEHIs) are protective against ischemia-induced lethal arrhythmias, but the mechanisms involved are unknown. Previously, we showed that sEHIs might reduce the incidence of ischemic arrhythmias by suppressing microRNA-1 (miR-1) in the myocardium. As miR-1 and miR-133 have the same proarrhythmic effects in the heart, we assumed that the beneficial effects of sEHIs might also relate to the regulation of miR-133.MethodsA mouse model of myocardial infarction (MI) was established by ligating the coronary artery. The sEHI t-AUCB (trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid) was administered daily for 7 days before MI. Myocardial infarct size and cardiac function was assessed at 24 h post-MI. The miRNA expression profiles of sham and MI mice treated with or without t-AUCB were determined by microarray and verified by real-time PCR. The incidence of arrhythmias was assessed by in vivo electrophysiologic studies. The mRNA levels of miR-133, its target genes (KCNQ1 [potassium voltage-gated channel subfamily Q member 1] and KCNH2 [potassium voltage-gated channel subfamily H member 2]), and serum response factor (SRF) were measured by real-time PCR; KCNQ1, KCNH2, and SRF protein levels were assessed by western blotting.ResultsWe demonstrated that the treatment with sEHIs could reduce infarct size, improve cardia function, and prevent the development of cardiac arrhythmias in MI mice. The expression levels of 14 miRNAs differed between the sham and MI groups. t-AUCB treatment altered the expression of eight miRNAs: two were upregulated and six were downregulated. Of these, the muscle-specific miR-133 was downregulated in the ischemic myocardium. In line with this, up-regulation of miR-133 and down-regulation of KCNQ1 and KCNH2 mRNA/protein were observed in ischemic myocaridum, whereas administration of sEHIs produced an opposite effect. In addition, miR-133 overexpression inhibited expression of the target mRNA, whereas t-AUCB reversed the effects. Furthermore, SRF might participate in the negative regulation of miR-133 by t-AUCB.ConclusionsIn MI mice, sEHI t-AUCB can repress miR-133, consequently stimulating KCNQ1 and KCNH2 mRNA and protein expression, suggesting a possible mechanism for its potential therapeutic application in ischemic arrhythmias.Electronic supplementary materialThe online version of this article (10.1186/s12944-018-0780-y) contains supplementary material, which is available to authorized users.

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Soluble epoxide hydrolase inhibitors, t-AUCB, regulated microRNA-1 and its target genes in myocardial infarction mice

Cited by 16 publications

References 37 publications

Potential Clinical Implications of miR-1 and miR-21 in Heart Disease and Cardioprotection

Potential Clinical Implications of miR-1 and miR-21 in Heart Disease and Cardioprotection

Potential roles of microRNA-1 and microRNA-133 in cardiovascular disease

Soluble epoxide hydrolase inhibitors, t-AUCB, downregulated miR-133 in a mouse model of myocardial infarction

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