The Role of Non-coding RNAs in Ischemic Myocardial Reperfusion Injury

Siebert, Vince; Allencherril, Joseph; Ye, Yumei; Wehrens, Xander H.T.; Birnbaum, Yochai

doi:10.1007/s10557-019-06893-x

Cited by 25 publications

(14 citation statements)

References 74 publications

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“…The expression of miRNAs undergoes changes in numerous disease states, including myocardial I/R injury (5). Studies have shown that some miRNAs promote fibrosis and apoptosis while others have opposite effects during myocardial I/R injury.…”

Section: Discussionmentioning

confidence: 99%

“…miRNAs are highly conserved and ubiquitously expressed in all species. There is evidence to suggest that miRNAs regulate necrotic, apoptotic and autophagic cardiomyocyte death by altering key signaling in myocardial I/R injury (4,5). For example, miR-494 targets pro-and antiapoptotic proteins to provide cardioprotective effects against I/R-induced injury via activation of the Akt pathway (6).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑145‑5p inhibits hypoxia/reoxygenation‑induced apoptosis in H9c2 cardiomyocytes by targeting ROCK1

Cheng

Liu³

et al. 2021

Exp Ther Med

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There is increasing evidence that microRNAs (miRs) play critical roles in the pathological and physiological processes associated with myocardial ischemia reperfusion (I/R). miR-145 has been extensively studied in the cardiovascular system; however, the role of miR-145 in myocardial I/R remains unclear. Therefore, the present study aimed to investigate the role and mechanism of miR-145-5p in myocardial I/R by establishing a hypoxia/reoxygenation (H/R) model using H9c2 cardiomyocytes. The expression of miR-145-5p was regulated by transfection and the potential target of miR-145-5p was identified. In addition, apoptosis of the cardiomyocytes was evaluated using flow cytometry and the detection of cleaved caspase-3 by western blotting. The results revealed that miR-145-5p expression was decreased while cell apoptosis and Rho-associated coiled-coil-containing kinase 1 (ROCK1) expression were increased in H/R-stimulated H9c2 cardiomyocytes. The upregulation of miR-145-5p reduced apoptosis and the expression of ROCK1 in H/R-stimulated H9c2 cardiomyocytes. Furthermore, the overexpression of ROCK1 significantly attenuated the miR-145-5p-induced reduction of apoptosis following H/R. In conclusion, the present study indicates that the overexpression of miR-145-5p inhibits H/R-induced cardiomyocyte apoptosis by targeting ROCK1.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA‑145‑5p inhibits hypoxia/reoxygenation‑induced apoptosis in H9c2 cardiomyocytes by targeting ROCK1

Cheng

Liu³

et al. 2021

Exp Ther Med

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“…miRNAs are a group of non-coding RNAs with 20-23 nucleotides in length, which perform to modulate gene expression, principally by repressing transcription or degrading messenger RNA (mRNA), and the relevance of miRNAs in mediating the cascade of myocardial IRI has been underscored previously [9]. miR-219a-1-3p was found to be one of the ten downregulated miRNAs in coronary artery disease [10].…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane attenuates cardiomyocyte apoptosis by mediating the miR-219a/AIM2/TLR4/MyD88 axis in myocardial ischemia/reperfusion injury in mice

Xing

Yuan

et al. 2020

Cell Cycle

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Myocardial infarction (MI) is a vital cause of death and disability globally. The primary treatment for diminishing acute myocardial ischemic injury is myocardial reperfusion, which may induce cardiomyocyte death. Our aim is to unravel the mechanism of sevoflurane (Sev) in microRNA-219a (miR-219a)-mediated regulation of absent in melanoma 2 (AIM2) and TLR4/MyD88 pathway during myocardial ischemia/reperfusion (I/R). The area of MI and apoptosis of cardiomyocytes of the developed mouse model were evaluated by TTC staining and TUNEL, respectively. After the determination of miR-219a as our target using microarray analysis, miR-219a atagomiR was used to treat the mouse model. The luciferase assay verified whether miR-219a targeted AIM2, and the miR-219a and AIM2 expression in myocardial tissues was detected by RT-qPCR and Western blot. miR-219a was significantly increased in myocardial tissues from mice treated with Sev, and the area of MI and cardiomyocyte apoptosis were decreased as a consequence. The miR-219a inhibitor reversed the action of Sev. Moreover, overexpression of AIM2 or induction of the TLR4 pathway aggravated myocardial I/R injury alleviated by miR-219a. All in all, the treatment of Sev upregulated miR-219a expression, which blocked the TLR4 pathway by targeting AIM2 and attenuated cardiomyocyte apoptosis in myocardial I/R mouse model.

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“…microRNAs (miRs) are acknowledged for their involvement in MIRI by serving as modulators of pivotal signaling factors [7]. During the various MIRI states, miRs are differentially expressed to influence the MIRI biological developments [8]. Additionally, the miR-130a ectopic expression reduces ROS production in patients with oxygen-glucose deprivation reperfusion (OGDR) [9], thereby exhibiting its protective properties in patients affected with diseases associated to ischemic reperfusion.…”

Section: Introductionmentioning

confidence: 99%

microRNA-130a-5p suppresses myocardial ischemia reperfusion injury by downregulating the HMGB2/NF-κB axis

Zhang

Zhanhu

et al. 2021

BMC Cardiovasc Disord

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Background Myocardial ischemia reperfusion injury (MIRI) is defined as tissue injury in the pathological process of progressive aggravation in ischemic myocardium after the occurrence of acute coronary artery occlusion. Research has documented the involvement of microRNAs (miRs) in MIRI. However, there is obscure information about the role of miR-130a-5p in MIRI. Herein, this study aims to investigate the effect of miR-130a-5p on MIRI. Methods MIRI mouse models were established. Then, the cardiac function and hemodynamics were detected using ultrasonography and multiconductive physiological recorder. Functional assays in miR-130a-5p were adopted to test the degrees of oxidative stress, mitochondrial functions, inflammation and apoptosis. Hematoxylin and eosin (HE) staining was performed to validate the myocardial injury in mice. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was employed to assess the expression patterns of miR-130a-5p, high mobility group box (HMGB)2 and NF-κB. Then, dual-luciferase reporter gene assay was performed to elucidate the targeting relation between miR-130a-5p and HMGB2. Results Disrupted structural arrangement in MIRI mouse models was evident from HE staining. RT-qPCR revealed that overexpressed miR-130a-5p alleviated MIRI, MIRI-induced oxidative stress and mitochondrial disorder in the mice. Next, the targeting relation between miR-130a-5p and HMGB2 was ascertained. Overexpressed HMGB2 annulled the protective effects of miR-130a-5p in MIRI mice. Additionally, miR-130a-5p targets HMGB2 to downregulate the nuclear factor kappa-B (NF-κB) axis, mitigating the inflammatory injury induced by MIRI. Conclusion Our study demonstrated that miR-130a-5p suppresses MIRI by down-regulating the HMGB2/NF-κB axis. This investigation may provide novel insights for development of MIRI treatments.

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The Role of Non-coding RNAs in Ischemic Myocardial Reperfusion Injury

Cited by 25 publications

References 74 publications

MicroRNA‑145‑5p inhibits hypoxia/reoxygenation‑induced apoptosis in H9c2 cardiomyocytes by targeting ROCK1

MicroRNA‑145‑5p inhibits hypoxia/reoxygenation‑induced apoptosis in H9c2 cardiomyocytes by targeting ROCK1

Sevoflurane attenuates cardiomyocyte apoptosis by mediating the miR-219a/AIM2/TLR4/MyD88 axis in myocardial ischemia/reperfusion injury in mice

microRNA-130a-5p suppresses myocardial ischemia reperfusion injury by downregulating the HMGB2/NF-κB axis

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