Abnormal expression of long non-coding RNAs in myocardial infarction

Wu, Tao; Wu, Huandong; Xu, Zhifei; Han, Fei; Zhang, Biqi; Sun, Jian; Hu, Shen‐Jiang

doi:10.1007/s00380-017-0990-7

Cited by 8 publications

(7 citation statements)

References 45 publications

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“…LncRNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) has been found to be up‐regulated in MI . Differentially expressed lnRNAs are determined in MI and co‐expressed with differentially expressed mRNAs, and their interactions are implicated in pathogenesis mechanism of MI . Silencing of ATP2B1‐AS1 can suppress renal interstitial fibrosis and oxidative stress in chronic renal failure .…”

Section: Discussionmentioning

confidence: 99%

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Song

Zhang

et al. 2020

J Cellular Molecular Medi

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Myocardial infarction (MI) is an acute coronary syndrome that refers to tissue infarction of the myocardium. This study aimed to investigate the effect of long intergenic non-protein-coding RNA (lincRNA) ATPase plasma membrane Ca 2+ transporting 1 antisense RNA 1 (ATP2B1-AS1) against MI by targeting nuclear factor-kappa-B inhibitor alpha (NFKBIA) and mediating the nuclear factor-kappa-B (NF-κB) signalling pathway. An MI mouse model was established and identified by cardiac function evaluation. It was determined that ATP2B1-AS1 was highly expressed, while NFKBIA was poorly expressed and NF-κB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1-AS1 vector, NFKBIA vector, siRNA-mouse ATP2B1-AS1 and siRNA-NFKBIA. The expression of NF-κBp50, NF-κBp65 and IKKβ was determined to identify whether ATP2B1-AS1 and NFKBIA affect the NF-κB signalling pathway, the results of which suggested that ATP2B1-AS1 down-regulated the expression of NFKBIA and activated the NF-κB signalling pathway in MI mice. Based on the data from assessment of cell viability, cell cycle, apoptosis and levels of inflammatory cytokines, either silencing of mouse ATP2B1-AS1 or overexpression of NFKBIA was suggested to result in reduced cardiomyocyte apoptosis and expression of inflammatory cytokines, as well as enhanced cardiomyocyte viability. Our study provided evidence that mouse ATP2B1-AS1 silencing may have the potency to protect against MI in mice through inhibiting cardiomyocyte apoptosis and inflammation, highlighting a great promise as a novel therapeutic target for MI. K E Y W O R D Smouse ATPase plasma membrane Ca 2+ transporting 1 antisense RNA 1, myocardial infarction, NF-kappa-B inhibitor alpha, nuclear factor-kappa-B signalling pathway | INTRODUC TI ONMyocardial infarction (MI) is a major public health concern that is commonly known as a heart attack characterized by a decline or complete stop of blood flow to the heart. 1 Since 1998, age-standardized AMI incidence decreased from 323 to 210 per 100 000 in 2007 in female and from 620 to 380 per 100 000 in 2007 in male, but socio-economic inequalities still exist in AMI incidence and have not narrowed. 2 In America, more than one million patients are | 4467 SONG et al.hospitalized due to MI annually, and the rates of readmission are approximately 20% within 30 days after discharge. 3 Moreover, the incidence of MI is increasing in China, and 23 million patients are estimated to experience MI by the end of 2030. 4 The risk factors of MI include hypertension, hypercholesterolaemia, diabetes, smoking habit, obesity, a sedentary lifestyle, excessive alcohol intake and unhealthy diet. 5,6 Earlier recognition or diagnosis of MI symptoms and prompt care-seeking actions are of great significance for the selection of the most appropriate treatments. 7 Although great improvements have been achieved in the prevention and therapies of MI, the difficulties in the prevention of MI are still steadily increasing. 8 Thus, further ef...

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Section: Discussionmentioning

confidence: 99%

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Song

Zhang

et al. 2020

J Cellular Molecular Medi

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“…Wu et al had demonstrated that differentially expressed lncRNAs had high connectivity with differentially expressed mRNAs in MI. 18 Cheng et al detected 26 pathways, some of which were important signaling pathways in myocardial infarction, including the Calcium signaling pathway and the MAPK signaling pathway. 17 KEGG pathway-enriched analysis of DEGs also indicated that the MAPK signaling pathway was remarkably enriched.…”

Section: Go Term Enrichment Analysis Of Degsmentioning

confidence: 99%

LINC-PINT Activates the Mitogen-Activated Protein Kinase Pathway to Promote Acute Myocardial Infarction by Regulating miR-208a-3p

Zhu¹,

et al. 2018

Circ J

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failure is highly generated. 4 Massive efforts are needed to improve the therapy of AMI.MicroRNAs (miRNAs) are a class of endogenic, non-coding single-stranded RNAs, approximately 21-25 nucleotides long. 5 MiRNAs participate in many biological processes such as cell growth, proliferation, apoptosis and differentiation, and many miRNAs have been reported to be indicated in various oncological and cardiovascular diseases. 6 Recent studies have shown that miR-1 and miR-208, which are the heart-specific or heart-enriched miRNAs, can be released into circulating blood after AMI. 7 The miR-208 family includes miR-208a, miR-208b and miR-499. MiR-208a is encoded by the intron of the

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“…Similarly, several studies have investigated the relationship between lncRNAs and AMI through expression profiling in myocardial infarction (MI) mice, but the findings of novel heart-specific lncRNAs were also diverse. For example, Ounzain 26 found 143 upregulated and 291 downregulated lncRNAs; however, 301 upregulated and 341 downregulated lncRNAs were reported in another study 27 . One might wonder why this phenomenon exists, and there are some possible reasons that can explain it.…”

Section: Discussionmentioning

confidence: 93%

Construction and analysis for differentially expressed long non-coding RNAs and mRNAs in acute myocardial infarction

Song

Luo

et al. 2020

Sci Rep

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Long noncoding RNAs (lncRNAs) are transcripts longer than 200 nucleotides. Some lncRNAs are related to acute myocardial infarction (AMI) and can serve as blood-based biomarkers for AMI detection. To identify whether new lncRNAs participate in AMI, the expression of lncRNAs and mRNAs was analysed by microarray analysis (Agilent human array) with the limma package in R in two series: five paired peripheral blood mononuclear cell (PBMC) samples and four paired plasma samples from different AMI patients. In PBMCs, a total of 2677 upregulated and 458 downregulated lncRNAs were significantly differentially expressed; additionally, 1168 mRNAs were upregulated and 1334 mRNAs were downregulated between the AMI patients and controls. In plasma, we found 41 upregulated and 51 downregulated lncRNAs that were differentially expressed, as well as 9 mRNAs that were upregulated and 9 mRNAs that were downregulated among the two groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using the clusterProfiler package in R, and differentially expressed mRNAs were functionally annotated. The top differentially expressed mRNAs were associated with circadian rhythm, the NF-kB pathway, the p53 pathway and the metabolism pathway. We further performed target gene prediction and coexpression analysis and revealed the interrelationships among the significantly differentially expressed lncRNAs and mRNAs. The expression of four lncRNAs (uc002ddj.1, NR_047662, ENST00000581794.1 and ENST00000509938.1) was validated in the newly diagnosed AMI and control groups by quantitative real-time PCR (qRT-PCR). Our study demonstrated that the clustered expression of lncRNAs between PBMCs and plasma showed tremendous differences. The newly screened lncRNAs may play indispensable roles in the development of AMI, although their biological functions need to be further validated. Acute myocardial infarction (AMI) continues to be the primary cause of disability and death, inducing a major health burden worldwide 1. In the last decade, therapeutic methods, such as coronary intervention, coronary artery bypass surgery and medications, have ameliorated the prognosis of AMI, although its mortality remains nearly as high as before. Thus, it is critical to initiate the early identification and risk stratification of AMI, which would greatly accelerate early intervention 2,3. Advances in genome-wide analyses, especially microarray profiling, play a potential role in discovering novel clinical biomarkers for AMI 4,5. Recently, in the field of AMI, long noncoding RNAs (lncRNAs) have attracted extensive attention. LncRNAs, ranging from 200 nucleotides to >10000 nucleotides in length 6 , lack protein coding capability since they have no open reading frames (ORFs). LncRNAs have been demonstrated to participate in specific physiological and pathological processes in a wide range of cardiovascular diseases (CVDs), such as heart failure 7-9 ,

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Abnormal expression of long non-coding RNAs in myocardial infarction

Cited by 8 publications

References 45 publications

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

Silencing of ATP2B1‐AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA‐mediated NF‐κB signalling pathway

LINC-PINT Activates the Mitogen-Activated Protein Kinase Pathway to Promote Acute Myocardial Infarction by Regulating miR-208a-3p

Construction and analysis for differentially expressed long non-coding RNAs and mRNAs in acute myocardial infarction

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