Downregulation of long non-coding RNA nuclear enriched abundant transcript 1 promotes cell proliferation and inhibits cell apoptosis by targeting miR-193a in myocardial ischemia/reperfusion injury

Ren, Lingyun; Chen, Shanshan; Liu, Wei; Hou, Pan; Sun, Wei; Hong, Yan

doi:10.1186/s12872-019-1122-3

Cited by 24 publications

(14 citation statements)

References 34 publications

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“…31 Overexpression of the lncRNA NEAT1 was also observed in myocardial I/R injury cells compared with normal myocardial cells. 32 The lncRNA MALAT1 showed more than fourfold higher expression in patients with T2DM compared with healthy controls. Among patients with T2DM, higher expression of the lncRNA MALAT1 was linked with weight loss, blurred vision, smoking, and alcoholism compared with the corresponding counterparts without these parameters.…”

Section: Discussionmentioning

confidence: 95%

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Circulating long non-coding RNAs NKILA, NEAT1, MALAT1, and MIAT expression and their association in type 2 diabetes mellitus

Alfaifi

Alshahrani

Ahmad

et al. 2021

BMJ Open Diab Res Care

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BackgroundType 2 diabetes mellitus (T2DM) is a multifactorial disorder that leads to alterations in gene regulation. Long non-coding RNAs (lncRNAs) have become a major research topic as they are involved in metabolic disorders.MethodsThis study included a total of 400 study subjects; 200 were subjects with T2DM and 200 were healthy subjects. Extracted RNA was used to synthesize cDNA by quantitative real time. Serum analysis was carried out to determine differences in biochemical parameters. Recorded data were used to evaluate associations with expression of lncRNAs NF-kappaB interacting lncRNA (NKILA), nuclear enriched abundant transcript 1 (NEAT1), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), and myocardial infarction-associated transcript (MIAT) in T2DM cases.ResultsCompared with healthy controls, patients with T2DM showed an overall increase in expression of lncRNAs NKILA, NEAT, MALAT1, and MIAT by 3.94-fold, 5.28-fold, 4.46-fold, and 6.35-fold, respectively. Among patients with T2DM, higher expression of lncRNA NKILA was associated with hypertension (p=0.001), smoking (p<0.0001), and alcoholism (p<0.0001). Altered NEAT1 expression was significantly associated with weight loss (p=0.04), fatigue (p=0.01), slow wound healing (p=0.002), blurred vision (p=0.008), loss of appetite (p=0.007), smoking (p<0.0001), and alcoholism (p<0.0001). Higher expression of lncRNA MALAT1 was significantly linked with weight loss (p=0.003), blurred vision (p=0.01), smoking (p<0.0001), and alcoholism (p<0.0001). Expression of lncRNA MIAT was associated with only blurred vision (p<0.0001), smoking (p<0.0001), and alcoholism (p<0.0001). Positive correlations of lncRNA NKILA with lncRNAs NEAT1 (r=0.42, p<0.0001), MALAT (r=0.36, p<0.0001) and MIAT (r=0.42, p<0.0001) were observed among patients with T2DM. Significant positive correlations of lncRNA NEAT with lncRNAs MALAT and MIAT were observed among patients with T2DM. A positive correlation between lncRNAs MALAT and MIAT was also observed among patients with T2DM.ConclusionIncreased circulating NKILA, NEAT1, MALAT, and MIAT expression in patients with T2DM, which is linked with poor patient outcomes and significantly linked with alcoholism and smoking, may influence the degree and severity of disease among patients with T2DM. These lncRNAs may contribute to the progression of T2DM disease or other related diabetes-related complications.

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Section: Discussionmentioning

confidence: 95%

“…31 Overexpression of the lncRNA NEAT1 was also observed in myocardial I/R injury cells compared with normal myocardial cells. 32 …”

Section: Discussionmentioning

confidence: 99%

Circulating long non-coding RNAs NKILA, NEAT1, MALAT1, and MIAT expression and their association in type 2 diabetes mellitus

Alfaifi

Alshahrani

Ahmad

et al. 2021

BMJ Open Diab Res Care

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“…There is increasing evidence that lncRNAs serve a significant role in the regulation of the myocardial IR process ( 68 ). For example, Ren et al ( 69 ) investigated the effect of lncRNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on cell proliferation and apoptosis in MIRI and observed that lnc-NEAT1 is overexpressed in MIRI compared with levels in normal cardiomyocytes. Downregulation of lnc-NEAT1 enhances cell proliferation and inhibits cell apoptosis by targeting miR-193a in IR injury H9C2 cells ( 69 ).…”

Section: Roles Of Hif-1α In Mirimentioning

confidence: 99%

“…For example, Ren et al ( 69 ) investigated the effect of lncRNA nuclear enriched abundant transcript 1 (lnc-NEAT1) on cell proliferation and apoptosis in MIRI and observed that lnc-NEAT1 is overexpressed in MIRI compared with levels in normal cardiomyocytes. Downregulation of lnc-NEAT1 enhances cell proliferation and inhibits cell apoptosis by targeting miR-193a in IR injury H9C2 cells ( 69 ). Li et al ( 70 ) assessed the role of lncRNA H19 in the regulation of MIRI and suggested that H19 expression levels are downregulated in IR hearts of mice and cardiomyocytes treated with H 2 O 2 .…”

Section: Roles Of Hif-1α In Mirimentioning

confidence: 99%

HIF‑1α in myocardial ischemia‑reperfusion injury (Review)

et al. 2021

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Myocardial ischemia-reperfusion injury (MIRI) is a severe injury to the ischemic myocardium following the recovery of blood flow. Currently, there is no effective treatment for MIRI in clinical practice. Over the past two decades, biological studies of hypoxia and hypoxia-inducible factor-1α (HIF-1α) have notably improved understanding of oxygen homeostasis. HIF-1α is an oxygen-sensitive transcription factor that mediates adaptive metabolic responses to hypoxia and serves a pivotal role in MIRI. In particular, previous studies have demonstrated that HIF-1α improves mitochondrial function, decreases cellular oxidative stress, activates cardioprotective signaling pathways and downstream protective genes and interacts with non-coding RNAs. The present review summarizes the roles and associated mechanisms of action of HIF-1α in MIRI. In addition, HIF-1α-associated MIRI intervention, including natural compounds, exosomes, ischemic preconditioning and ischemic post-processing are presented. The present review provides evidence for the roles of HIF-1α activation in MIRI and supports its use as a therapeutic target. Contents 1. Introduction 2. Molecular characteristics of HIF-1α 3. HIF-1α-mediated transcriptional responses to hypoxia 4. Roles of HIF-1α in MIRI 5. Involvement of HIF-1α in the myocardial protective effects of natural compounds against MIRI 6. Roles of HIF-1α in myocardial ischemic pre-and post-conditioning 7. Future perspectives

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“…Previous studies have reported that non-coding RNAs serve an important role in regulating pathophysiological processes of myocardial I/R injury, including cell differentiation, proliferation, apoptosis, necrosis and autophagy ( 4 – 7 ). Non-coding RNAs are functional RNAs that are transcribed from non-coding DNAs and have important regulatory functions, although they lack the potential of protein coding ( 8 ).…”

Section: Introductionmentioning

confidence: 99%

Differentially expressed lncRNAs, miRNAs and mRNAs with associated ceRNA networks in a mouse model of myocardial ischemia/reperfusion injury

et al. 2020

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Non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs/miRs), have significant regulatory effects on a number of biological processes in myocardial ischemia/reperfusion (I/R) injury, including cell differentiation, proliferation and apoptosis. In the present study, the expression levels of lncRNAs, miRNAs and mRNAs were evaluated in a mouse model of myocardial I/R injury. The potential functions of these differentially expressed genes were then analyzed via Gene Ontology and pathway analyses. Additionally, the interactions between lncRNA-miRNA-mRNA were predicted by constructing a competing endogenous RNA regulatory network. It was found that 14,366 lncRNAs, 151 miRNAs and 9,377 mRNAs were differentially expressed in mice hearts after I/R compared with the Sham group (fold change >2; P<0.05). The results indicated that these differentially expressed genes were involved in multiple molecular functions, including ‘guanosine diphosphate binding’, ‘RNA polymerase II carboxy-terminal domain kinase activity’, ‘TATA-binding protein-class protein binding’, ‘nicotinamide adenine dinucleotide binding’ and ‘protein phosphatase type 2A regulator activity’. The interactions between lncRNA-miRNA-mRNA, including five lncRNAs, 38 miRNAs and 196 mRNAs, were predicted, specifically Gm12040-mmu-miR-125a-5p-decapping mRNA 1B, Rpl7l1-ps1-mmu-miR-124-3p-G protein-coupled receptor 146, Gm11407-mmu-miR-190a-5p-homeobox and leucine zipper encoding (HOMEZ), 1600029O15Rik-mmu-miR-132-3p-HOMEZ and AK155692-mmu-miR-1224-3p-activating transcription factor 6β. Collectively, these findings provided novel insights for future research on lncRNAs, miRNAs and mRNAs in myocardial I/R injury.

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Downregulation of long non-coding RNA nuclear enriched abundant transcript 1 promotes cell proliferation and inhibits cell apoptosis by targeting miR-193a in myocardial ischemia/reperfusion injury

Cited by 24 publications

References 34 publications

Circulating long non-coding RNAs NKILA, NEAT1, MALAT1, and MIAT expression and their association in type 2 diabetes mellitus

Circulating long non-coding RNAs NKILA, NEAT1, MALAT1, and MIAT expression and their association in type 2 diabetes mellitus

HIF‑1α in myocardial ischemia‑reperfusion injury (Review)

Differentially expressed lncRNAs, miRNAs and mRNAs with associated ceRNA networks in a mouse model of myocardial ischemia/reperfusion injury

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