miR-361-3p mitigates hypoxia-induced cardiomyocyte injury via targeting apoptosis initiators caspase-2/-8/-9

Zhang, Jinwei; Zhou, Xiankun; Sun, Jing; Li, Mingzhou; Ma, Jideng; Ge, Liangpeng

doi:10.1007/s11626-021-00644-9

Cited by 6 publications

(2 citation statements)

References 21 publications

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“…To explore the mechanism function of MIAT, we used the starBase database to predict its targeted miRNAs. Among these candidates, three miRNAs (miR‐361‐3p, miR‐488‐3p, and miR‐188‐5p) were found to possess cardio‐protective functions (Chen et al, 2020; J. Zhang, Zhou, et al, 2022; Zheng et al, 2019). By qRT‐PCR analysis, we observed that only miR‐488‐3p expression was elevated in MIAT‐silenced AC16 cells (Supporting Information: Figure 5), suggesting the direct relationship between miR‐488‐3p and MIAT.…”

Section: Resultsmentioning

confidence: 99%

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Knockdown of long noncoding RNA MIAT attenuates hypoxia‐induced cardiomyocyte injury by regulating the miR‐488‐3p/Wnt/β‐catenin pathway

Zhang

et al. 2022

Cell Biology International

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Dysfunction of cardiomyocytes contributes to the development of acute myocardial infarction (AMI). Nonetheless, the regulatory mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in cardiomyocyte injury remains largely unclear. The cardiomyocyte injury was assessed via cell viability and apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and flow cytometry, respectively. The levels of MIAT, microRNA (miR)-488-3p, and Wnt5a were detected via quantitative real-time polymerase chain reaction and Western blot.After bioinformatical analysis, the binding between miR-488-3p and MIAT or Wnt5a was confirmed via dual-luciferase reporter, RNA immunoprecipitation, and RNA pulldown assays. Our results showed that MIAT expression was increased in AC16 cells after hypoxia treatment. Silencing of MIAT alleviated hypoxia-induced viability reduction, apoptosis increase, and Wnt/β-catenin pathway activation. MIAT directly targeted miR-488-3p. MiR-488-3p might repress hypoxia-induced cardiomyocyte injury, and its knockdown reversed the effect of MIAT depletion on cardiomyocyte injury. Wnt5a was validated as a target of miR-488-3p. Wnt5a expression restoration attenuated the influence of MIAT knockdown on hypoxia-triggered cardiomyocyte injury. Our findings demonstrated that downregulation of MIAT might mitigate hypoxia-induced cardiomyocyte injury partly through miR-488-3p mediated Wnt/β-catenin pathway.

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Section: Resultsmentioning

confidence: 99%

“…J. Zhang, Zhou, et al, 2022;Zheng et al, 2019). By qRT-PCR analysis, we observed that only miR-488-3p expression was elevated in MIAT-silenced AC16 cells (Supporting Information:…”

Section: Mir-488-3p a Target Of Miat Represses Cardiomyocyte Injury I...mentioning

confidence: 99%

Knockdown of long noncoding RNA MIAT attenuates hypoxia‐induced cardiomyocyte injury by regulating the miR‐488‐3p/Wnt/β‐catenin pathway

Zhang

et al. 2022

Cell Biology International

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Unveiling caspase-2 regulation by non-coding RNAs

2022

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Non-coding RNAs (ncRNAs) are a group of RNA molecules, such as small nucleolar RNAs, circular RNAs (circRNAs), microRNAs (miRNAs) and long-noncoding RNAs (ncRNAs), that do not encode proteins. Although their biofunctions are not well-understood, many regulatory ncRNAs appear to be highly involved in regulating the transcription and translation of several genes that have essential biological roles including cell differentiation, cell death, metabolism, tumorigenesis and so on. A growing number of studies have revealed the associations between dysregulated ncRNAs and caspases involved in cell death in numerous human diseases. As one of the initiator and executor caspases, caspase-2 is the most evolutionally conserved caspase in mammals, exerting both apoptotic and non-apoptotic functions. A great deal of studies has shown the involvement of caspase-2 as a tumor suppressor in multiple oncogene-driven cancers, and yet a comprehensive understanding of its biological roles remains largely unknown. In this review, we highlight a compilation of studies focused on the interaction between caspase-2 and miRNAs/lncRNAs in the context of different diseases in order to deepen our knowledge on the regulatory biofunctions of caspase-2 and, furthermore, provide more insight into understanding the role that ncRNAs/caspase-2 axis plays in the development of human diseases.

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miR-361-3p overexpression promotes apoptosis and inflammation by regulating the USP49/IκBα/NF-κB pathway to aggravate sepsis-induced myocardial injury

Geng,

Qi,

You

et al. 2024

Toxicology Research

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Background Sepsis is a major cause of in-hospital death, particularly in the intensive care unit. A huge amount of effort has been put into identifying reliable biomarkers to improve the prognosis of patients with sepsis. Among the numerous candidates, microRNAs have attracted attention because of their promising prognostic value. Multiple miRNAs have been suggested to play vital roles in manipulating the nuclear factor-kappa B (NF-κB) pathway, a key factor involved in sepsis. In this study, we attempted to elucidate the potential functions of miR-361-3p in sepsis-induced myocardial injury in vivo and in vitro. Methods A sepsis model was established by cecal ligation and puncture (CLP) in rats and by lipopolysaccharide (LPS) in H9c2 cells. The functions of miR-361-3p were revealed by assessing the level of biomarkers of myocardial injury and inflammation by Enzyme-linked immunosorbent assay, as well as the apoptosis by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and flow cytometry. Binding of miR-361-3p and the 3′ untranslated region of ubiquitin-specific peptidase 49 (Usp49) was revealed by Dual luciferase reporter gene assay. The interaction of USP49 and its downstream target NF-κB inhibitor alpha (IκBα) was revealed by Co-immunoprecipitation and western blot analysis. Results miR-361-3p antagomir inhibited myocardial injury and inflammation in CLP-induced rats, as evidenced by a decrease in the serum levels of cardiac troponin I, creatine kinase-MB, interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha and cell apoptosis. However, miR-361-3p agomir aggravated sepsis-induced myocardial injury. Moreover, miR-361-3p inhibition induced the inhibition of LPS-induced apoptosis and inflammation in H9c2 cells. miR-361-3p could inhibit the expression of Usp49 by binding to its 3′ untranslated region. Furthermore, we demonstrated that Usp49 binds to IκBα and mediates its deubiquitination, leading to the stabilization of IκBα, which results in the cytoplasmic accumulation of NF-κB and eventually the suppression of NF-κB activity. Conclusion Taken together, our data demonstrate that miR-361-3p overexpression promotes apoptosis and inflammation by regulating the USP49/IκBα/NF-κB pathway to aggravate sepsis-induced myocardial injury.

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miR-361-3p mitigates hypoxia-induced cardiomyocyte injury via targeting apoptosis initiators caspase-2/-8/-9

Cited by 6 publications

References 21 publications

Knockdown of long noncoding RNA MIAT attenuates hypoxia‐induced cardiomyocyte injury by regulating the miR‐488‐3p/Wnt/β‐catenin pathway

Knockdown of long noncoding RNA MIAT attenuates hypoxia‐induced cardiomyocyte injury by regulating the miR‐488‐3p/Wnt/β‐catenin pathway

Unveiling caspase-2 regulation by non-coding RNAs

miR-361-3p overexpression promotes apoptosis and inflammation by regulating the USP49/IκBα/NF-κB pathway to aggravate sepsis-induced myocardial injury

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