Differential Expression Profiles and Functional Analysis of Circular RNAS in Children with Fulminant Myocarditis

Zhang, Li; Han, Bo; Wang, Jing; Liu, Qingqing; Kong, Yaru; Jiang, Diandong; Jia, Honglei

doi:10.2217/epi-2019-0101

Cited by 16 publications

(15 citation statements)

References 41 publications

(44 reference statements)

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“…Many researchers have found that circRNAs play an important role in cardiovascular diseases such as myocardial infarction, heart failure, and atherosclerosis (Wang K. et al, 2016 ; Wang et al, 2017 ; Zhang F. et al, 2018 ). Zhang et al confirmed that circRNAs were differentially expressed in fulminant myocarditis, and further bioinformatic analysis showed that many inflammatory or immune pathways, including TNF signaling pathway, Th1 and Th2 cell differentiation and T cell receptor signaling pathway, were involved in VMC (Zhang L. et al, 2019 ). Therefore, circRNAs may be a new therapeutic target for VMC by regulating the immune-inflammatory pathway.…”

Section: The Role Of Circrnas In Vmcmentioning

confidence: 97%

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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Section: The Role Of Circrnas In Vmcmentioning

confidence: 97%

The Role of Non-coding RNAs in Viral Myocarditis

Zhang

Xiong

Zeng

et al. 2020

Front. Cell. Infect. Microbiol.

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“…These targeted pathways are known, critical mediators for the clinical outcomes for SARS-CoV-2-infected patients and give us insight about virus pathophysiology. It is well established that for enveloped viruses, such as SARS-CoV-2, N-or O-glycosylation of S protein determines the viral entry and membrane fusion with functional elicitation of host immune responses [46]. The high-resolution LC-MS/MS experiment was performed to detect site-specific quantitative N-linked and O-linked glycan profiling on SARS-CoV-2 subunit S1 and S2 proteins.…”

Section: Mir-8066mentioning

confidence: 99%

The Prediction of miRNAs in SARS-CoV-2 Genomes: hsa-miR Databases Identify 7 Key miRs Linked to Host Responses and Virus Pathogenicity-Related KEGG Pathways Significant for Comorbidities

Arısan

Dart

Grant

et al. 2020

Viruses

101

165

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Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a member of the betacoronavirus family, which causes COVID-19 disease. SARS-CoV-2 pathogenicity in humans leads to increased mortality rates due to alterations of significant pathways, including some resulting in exacerbated inflammatory responses linked to the “cytokine storm” and extensive lung pathology, as well as being linked to a number of comorbidities. Our current study compared five SARS-CoV-2 sequences from different geographical regions to those from SARS, MERS and two cold viruses, OC43 and 229E, to identify the presence of miR-like sequences. We identified seven key miRs, which highlight considerable differences between the SARS-CoV-2 sequences, compared with the other viruses. The level of conservation between the five SARS-CoV-2 sequences was identical but poor compared with the other sequences, with SARS showing the highest degree of conservation. This decrease in similarity could result in reduced levels of transcriptional control, as well as a change in the physiological effect of the virus and associated host-pathogen responses. MERS and the milder symptom viruses showed greater differences and even significant sequence gaps. This divergence away from the SARS-CoV-2 sequences broadly mirrors the phylogenetic relationships obtained from the whole-genome alignments. Therefore, patterns of mutation, occurring during sequence divergence from the longer established human viruses to the more recent ones, may have led to the emergence of sequence motifs that can be related directly to the pathogenicity of SARS-CoV-2. Importantly, we identified 7 key-microRNAs (miRs 8066, 5197, 3611, 3934-3p, 1307-3p, 3691-3p, 1468-5p) with significant links to KEGG pathways linked to viral pathogenicity and host responses. According to Bioproject data (PRJNA615032), SARS-CoV-2 mediated transcriptomic alterations were similar to the target pathways of the selected 7 miRs identified in our study. This mechanism could have considerable significance in determining the symptom spectrum of future potential pandemics. KEGG pathway analysis revealed a number of critical pathways linked to the seven identified miRs that may provide insight into the interplay between the virus and comorbidities. Based on our reported findings, miRNAs may constitute potential and effective therapeutic approaches in COVID-19 and its pathological consequences.

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“…In addition, the microarray data revealed that MAPK14 was upregulated in MC. Based on these intriguing findings, we hypothesized that hsa_circ_0071542 might regulate the expression of MAPK14 by binding to hsa-miR-8055 through the interactions of circRNA-miRNA-mRNA network 42 . Hsa_circ_0071542 is derived from the ACSL1 pre-mRNA transcript.…”

Section: Introductionmentioning

confidence: 99%

“…Our previous investigations have provided a comprehensive expression profile of differentially expressed circRNAs, among which the expression of hsa_circ_0071542 was significantly ( p < 0.05) upregulated in children with FM pathology 42 . This result was further validated by microarray analysis and quantitative real-time polymerase chain reaction (qRT-PCR) assay as well.…”

Section: Introductionmentioning

confidence: 99%

Circular RNA circACSL1 aggravated myocardial inflammation and myocardial injury by sponging miR-8055 and regulating MAPK14 expression

et al. 2021

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Myocarditis (MC) is a common, potentially life-threatening inflammatory disease of the myocardium. A growing body of evidence has shown that mitogen-activated protein kinase 14 (MAPK14) participates in the pathogenesis of MC. However, the upstream regulators of MAPK14 remain enigmatic. Circular RNAs (circRNAs) have been identified to play vital roles in the pathophysiology of cardiovascular diseases. Nevertheless, the clinical significance, biological function, and regulatory mechanisms of circRNAs in MC remain poorly understood. In this study, we determined a novel circRNA, circACSL1 (ID: hsa_circ_0071542), which was significantly upregulated in the acute phase of MC, and its dynamic change in expression was related to the progression of MC. We used lipopolysaccharide (LPS) to induce the inflammatory responses in the human cardiomyocytes (HCM) line for in vitro and in cellulo experiments. The pro-inflammatory factors (IL-1β, IL-6, and TNF-α), myocardial injury markers (cTnT, CKMB, and BNP), cell viability, and cell apoptosis were measured to evaluate the extent of myocardial inflammation and myocardial injury level. Functional experiments, including gain-of-function and loss-of-function, were then performed to investigate the pro-inflammatory roles of circACSL1. The results revealed that circACSL1 could aggravate inflammation, myocardial injury, and apoptosis in HCM. Mechanistically, circACSL1 acted as a sponge for miR-8055-binding sites to regulate the downstream target MAPK14 expression. Furthermore, overexpression of miR-8055 rescued the pro-inflammatory effects of circACSL1 on HCM, and the upregulation of MAPK14 induced by circACSL1 was attenuated by miR-8055 overexpression. Knockdown of circACSL1 or overexpression of miR-8055 reduced myocardial inflammation and myocardial injury level and these effects were rescued by overexpression of MAPK14. In summary, our study demonstrated that circACSL1 could aggravate myocardial inflammation and myocardial injury through competitive absorption of miR-8055, thereby upregulating MAPK14 expression. Moreover, circACSL1 may represent a potential novel biomarker for the precise diagnosis of MC and offer a promising therapeutic target for MC treatment.

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Differential Expression Profiles and Functional Analysis of Circular RNAS in Children with Fulminant Myocarditis

Cited by 16 publications

References 41 publications

The Role of Non-coding RNAs in Viral Myocarditis

The Role of Non-coding RNAs in Viral Myocarditis

The Prediction of miRNAs in SARS-CoV-2 Genomes: hsa-miR Databases Identify 7 Key miRs Linked to Host Responses and Virus Pathogenicity-Related KEGG Pathways Significant for Comorbidities

Circular RNA circACSL1 aggravated myocardial inflammation and myocardial injury by sponging miR-8055 and regulating MAPK14 expression

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