Expression of miR-98 in myocarditis and its influence on transcription of the FAS/FASL gene pair

Zhang, B Y; Zhao, Zhigang; Jin, Zhe

doi:10.4238/gmr.15027627

Cited by 15 publications

(12 citation statements)

References 15 publications

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“…In contrast, Zhang et al found that miR-98 was downregulated in patients with myocarditis, whereas the expression of FAS/FASL was increased 1.68-fold. After performing experiments in cell culture, the authors found that miR-98 targets the FAS/FASL gene pair which can induce apoptosis [41].…”

Section: Resultsmentioning

confidence: 99%

MicroRNAs in Inflammatory Heart Diseases and Sepsis-Induced Cardiac Dysfunction: A Potential Scope for the Future?

Mirna

Paar

Rezar

et al. 2019

Cells

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Background: MicroRNAs (miRNAs) are small, single-stranded RNA sequences that regulate gene expression on a post-transcriptional level. In the last few decades, various trials have investigated the diagnostic and therapeutic potential of miRNAs in several disease entities. Here, we provide a review of the available evidence on miRNAs in inflammatory heart diseases (myocarditis, endocarditis, and pericarditis) and sepsis-induced cardiac dysfunction. Methods: Systematic database research using the PubMed and Medline databases was conducted between July and September 2019 using predefined search terms. The whole review was conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Results: In total, 131 studies were screened, 96 abstracts were read, and 69 studies were included in the review. Discussion: In the future, circulating miRNAs could serve as biomarkers for diagnosis and disease monitoring in the context of inflammatory heart diseases and sepsis-induced cardiac dysfunction. Considering the promising results of different animal models, certain miRNAs could also emerge as novel therapeutic approaches in this setting.

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Section: Resultsmentioning

confidence: 99%

MicroRNAs in Inflammatory Heart Diseases and Sepsis-Induced Cardiac Dysfunction: A Potential Scope for the Future?

Mirna

Paar

Rezar

et al. 2019

Cells

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“…Then the researchers confirmed miR-34a act as a pro-apoptotic molecule in VMC via targeting the SIRT1-p53 signaling pathway (Jiang et al, 2019 ). In contrast, miR-222, miR-98, and miR-21 may act as anti-apoptotic factors in VMC (He et al, 2013 ; Zhang B. Y. et al, 2016 ; Zhang X. et al, 2019 ). Zhang et al found that the expression of adenosine deaminase, RNA-specific (ADAR1) and miR-222 was increased in CVB3 induced VMC model, and the study in vitro showed that ADAR1 combined Dicer increased cell viability by inducing miR-222 synthesis which decreased the confirmed target phosphatase and tensin homolog (PTEN) expression (Zhang X. et al, 2019 ).…”

Section: The Role Of Mirnas In Cvb3-induced Vmcmentioning

confidence: 99%

“…Hence, ADAR1-Dicer Complex may inhibit cell apoptosis by miR-222 in CVB3 induced VMC. Additionally, MiR-98 decreased cell apoptosis by targeting the FAS/FASL gene (Zhang B. Y. et al, 2016 ), and miR-21 reduced cell apoptosis by targeting programmed cell death 4 (PDCD4) (He et al, 2013 ), a well-known apoptosis gene (Gaur et al, 2011 ; Stagakis et al, 2011 ; Junker et al, 2015 ). Furthermore, another study confirmed that miR-21 reduced cell apoptosis by targeting mitogen-activated protein kinase kinase 3 (MAP2K3) (He et al, 2019 ).…”

Section: The Role Of Mirnas In Cvb3-induced Vmcmentioning

confidence: 99%

The Role of Non-coding RNAs in Viral Myocarditis

Zhang

Xiong

Zeng

et al. 2020

Front. Cell. Infect. Microbiol.

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Viral myocarditis (VMC) is a disease characterized as myocardial parenchyma or interstitium inflammation caused by virus infection, especially Coxsackievirus B3 (CVB3) infection, which has no accurate non-invasive examination for diagnosis and specific drugs for treatment. The mechanism of CVB3-induced VMC may be related to direct myocardial damage of virus infection and extensive damage of abnormal immune response after infection. Non-coding RNA (ncRNA) refers to RNA that is not translated into protein and plays a vital role in many biological processes. There is expanding evidence to reveal that ncRNAs regulate the occurrence and development of VMC, which may provide new treatment or diagnosis targets. In this review, we mainly demonstrate an overview of the potential role of ncRNAs in the pathogenesis, diagnosis and treatment of CVB3-induced VMC.

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“…miRNAs have emerged as key regulators of the immune system, which protect myocarditis against various stimulations by inhibiting apoptosis or targeting nuclear factor kappa-B. [26][27][28] miR-223 was initially described as a modulator of hematopoietic lineage differentiation. 29) Many studies have illustrated that miR-223 can be used as a new potential target for the diagnosis and treatment of inflammatory diseases, such as atopic dermatitis, 30) immune-mediated neuroinflammatory diseases, 31) and acute lung injury.…”

Section: Discussionmentioning

confidence: 99%

Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

Yang¹,

Jiang²,

Zhuge³

2019

Int. Heart J.

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Emodin is a natural product extracted from Rheum palmatum. There are few recent studies on emodin in the treatment of myocarditis. This study aimed to investigate the effect of emodin on lipopolysaccharide (LPS)induced inflammatory injury in cardiomyocytes. H9c2 cells were treated with 10 μM of LPS and different concentrations (0, 1, 5, 10, 15, and 20 μM) of emodin. The expression of miR-223 was changed by transient transfection. Thereafter, cell viability, apoptosis, the expression of CyclinD1 and Jnk-associated proteins, and the release of pro-inflammatory factors were assessed by cell Counting Kit-8, flow cytometry analysis, quantitative real-time polymerase chain reaction Western blot, and enzyme-linked immunosorbent assay respectively. The results showed that 20 μM of emodin significantly decreased H9c2 cells viability. LPS significantly damaged H9c2 cells, as cell viability was reduced, CyclinD1 was down-regulated, apoptosis was induced, the release of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-alpha were increased, and the phosphorylation of Jnk and c-Jun were promoted. Emodin protected H9c2 cells against LPS-induced inflammatory injury. miR-223 expression was significantly up-regulated by LPS exposure, while emodin lessened this up-regulation. LPS-injured H9c2 cells were attenuated by the overexpression of miR-223; emodin has protective actions on LPS-injured H9c2 cells and targets. Besides, SP600125 (an inhibitor of Jnk) eliminated miR-223-modulated inflammatory injury in H9c2 cells. These data demonstrated that emodin could attenuate LPS-induced inflammatory injury and deactivate Jnk signaling pathway through down-regulation of miR-223. (Int Heart J 2019; 60: 436-443)

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Expression of miR-98 in myocarditis and its influence on transcription of the FAS/FASL gene pair

Cited by 15 publications

References 15 publications

MicroRNAs in Inflammatory Heart Diseases and Sepsis-Induced Cardiac Dysfunction: A Potential Scope for the Future?

MicroRNAs in Inflammatory Heart Diseases and Sepsis-Induced Cardiac Dysfunction: A Potential Scope for the Future?

The Role of Non-coding RNAs in Viral Myocarditis

Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

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