Plasma miR-122 and miR-3149 Potentially Novel Biomarkers for Acute Coronary Syndrome

Li, Xiangdong; Yang, Yuejin; Wang, Laiyuan; Qiao, Shubin; Lu, Xiangfeng; Wu, Yongjian; Xu, Biao; Li, Hongfan; Gu, Dongfeng

doi:10.1371/journal.pone.0125430

Cited by 38 publications

(32 citation statements)

References 30 publications

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“…Due to lack of clarity in the results of the groups compared and results presented in Li (2015), 29 this study was not included in the summaries below.…”

Section: Resultsmentioning

confidence: 99%

Identifying circulating microRNAs as biomarkers of cardiovascular disease: a systematic review

et al. 2016

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The aim of the present study is to identify microRNAs (miRs) with high potential to be used as biomarkers in plasma and/or serum to clinically diagnose, or provide accurate prognosis for survival in, patients with atherosclerosis, coronary artery disease, and acute coronary syndrome (ACS). A systematic search of published original research yielded a total of 72 studies. After review of the risk of bias of the published studies, according to Cochrane Collaboration and the QUADUAS Group standards, 19 studies were selected. Overall 52 different miRs were reported. In particular, miR-133a/b (5 studies), miR-208a/b (6 studies), and miR-499 (7 studies) were well studied and found to be significant diagnostic and/or prognostic markers across different cardiovascular disease progression stages. miR-1 and miR-145b are potential biomarkers of ACS; miR-1 with higher sensitivity for all acute myocardial infarction (AMI), and miR-145 for STEMI and worse outcome of AMI. But when miRs were studied across different ACS study populations, patients had varying degrees of coronary stenosis, which was identified as an important confounder that limited the ability to quantitatively pool the study results. The identified miRs were found to regulate endothelial function and angiogenesis (miR-1, miR-133), vascular smooth muscle cell differentiation (miR-133, miR-145), communication between vascular smooth muscle and endothelial cell to stabilize plaques (miR-145), apoptosis (miR-1, miR-133, miR-499), cardiac myocyte differentiation (miR-1, miR-133, miR-145, miR-208, miR-499), and to repress cardiac hypertrophy (miR-133). Their role in these processes may be explained by regulation of shared RNA targets such as cyclin-dependent kinase inhibitor 1A (or p21), ETS proto-oncogene 1, fascin actin-bundling protein 1, hyperpolarization-activated cyclic nucleotide-gated potassium channel 4, insulin-like growth factor 1 receptor LIM and SH3 protein 1, purine nucleoside phosphorylase, and transgelin 2. These mechanistic data further support the clinical relevance of the identified miRs. miR-1, miR-133a/b, miR-145, miR-208a/b, and miR-499(a) in plasma and/or serum show some potential for diagnosis of cardiovascular disease. However, biased selection of miRs in most studies and unexplained contrasting results are major limitations of current miR research. Inconsistencies need to be addressed in order to definitively identify clinically useful miRs. Therefore, this paper presents important aspects to improve future miR research, including unbiased selection of miRs, standardization/normalization of reference miRs, adjustment for patient comorbidities and medication, and robust protocols of data-sharing plans that could prevent selective publication and selective reporting of miR research outcomes.

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“…Due to lack of clarity in the results of the groups compared and results presented in Li (2015), 29 this study was not included in the summaries below.…”

Section: Resultsmentioning

confidence: 99%

Identifying circulating microRNAs as biomarkers of cardiovascular disease: a systematic review

et al. 2016

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“…Karakas et al [23] shows that miR-140-3p derived from peripheral blood predicts mortality, and thus could be a valuable biomarker for risk estimation in coronary artery disease. Recent studies indicate that miR-140-3p is significantly elevated during early stages of acute coronary syndrome [24,25], and elevated plasma miR-140-3p in patients with acute coronary syndrome mainly originates from circulating endothelial cells and lymphocytes [24]. Li et al [26] reported that knockdown of miR-140 reduced myocardial infarct sizes in an animal model, whereas miR-140 was upregulated upon apoptotic stimulation.…”

Section: Discussionmentioning

confidence: 99%

Circulating miRNA Expression Profiling and Target Prediction in Patients Receiving Dexmedetomidine

Yang

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Circulating miRNAs could serve as biomarkers for diagnosis or prognosis of heart diseases and cerebrovascular diseases. Dexmedetomidine has protective effects in various organs. The effects of dexmedetomidine on circulating miRNAs remain unknown. Here, we investigated differentially expressed miRNA and to predict the target genes of the miRNA in patients receiving dexmedetomidine. Methods: The expression levels of circulating miRNAs of 3 patients were determined through high through-put miRNA sequencing technology. Target genes of the identified differentially expressed miRNAs were predicted using TargetScan 7.1 and miRDB v.5. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to conduct functional annotation and pathway enrichment analysis of target genes respectively. Results: Twelve differentially expressed miRNAs were identified. Five miRNAs were upregulated (hsa-miR-4508, hsa-miR-novel-chr8_87373, hsa-miR-30a-3p, hsa-miR-novel-chr16_26099, hsa-miR-4306) and seven miRNAs (hsa-miR-744-5p, hsa-miR-320a, hsa-miR-novel-chr9_90035, hsa-miR-101-3p, hsa-miR-150-5p, hsa-miR-342-3p, and hsa-miR-140-3p) were downregulated after administration of dexmedetomidine in the subjects. The target genes and pathways related to the differentially expressed miRNAs were predicted and analyzed. Conclusion: The differentially expressed miRNAs may be involved in the mechanisms of action of dexmedetomidine. Specific miRNAs, such as hsa-miR-101-3p, hsa-miR-150-5p and hsa-miR-140-3p, are new potential targets for further functional studies of dexmedetomidine.

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“…[25][26][27][28] A previous study has shown that miR-122 regulates apoptosis in cutaneous TCell lymphoma through the p53/Akt signaling pathway. 40 Additionally, miR-122 has been found to promote cardiac apoptosis in Pax-8-/-mice and to affect CCK-8 expression in H9c2 cells.…”

Section: Discussionmentioning

confidence: 99%

“…[20][21][22][23] In our previous study, 24 the differential miRNA prole in a rat model of post-infarction heart failure showed that miR-122, as one of the most abundantly expressed miRNAs, is markedly upregulated during the development of heart failure, which revealed its potential role in this complex pathological process. Furthermore, miR-122 has been applied as a novel biomarker for many cardiovascular diseases such as acute coronary syndrome [25][26][27][28] and as a predictor of outcome. 29 However, whether miR-122 involves in Ang II-induced apoptosis and the mechanisms by which miR-122 contributes to apoptosis remain unclear.…”

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confidence: 99%

The impact of microRNA-122 and its target gene Sestrin-2 on the protective effect of ghrelin in angiotensin II-induced cardiomyocyte apoptosis

et al. 2018

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Ghrelin with n-octanoylated serine 3 residue is a peptide hormone with well-known cardioprotective properties.MicroRNA-122 is associated with the pathogenesis of many cardiovascular diseases, including apoptosis and was found highly increased in our previous rat model of post-myocardial infarction heart failure. In this study, we aimed to identify the target gene of microRNA-122 and to evaluate their impacts on the protective effect of acylated ghrelin in angiotensin II-induced apoptosis. The results showed that microRNA-122 was upregulated in the angiotensin II administration group accompanied by increased cell apoptosis, which were both reversed by ghrelin. Furthermore, microRNA-122 mimics upregulated numerous pro-apoptotic genes and increased apoptosis. The luciferase activity assay revealed Sestrin-2 as a direct target of microRNA-122.The expression of Sestrin-2 was downregulated by angiotensin II and upregulated by co-treatment with ghrelin. Inhibition of microRNA-122 and overexpression of Sestrin-2 alleviated apoptosis which was further reduced upon administered of ghrelin. Together, these results indicated that Sestrin-2 expression is inhibited by microRNA-122 and that this inhibition is involved in the protective effect of ghrelin and angiotensin II-induced apoptosis. We also found that microRNA-122 influenced several apoptosis pathways including the caspase cascade reaction and death receptor-mediated pathways. Collectively, our data reveal that microRNA-122 and its target gene Sestrin-2, under the regulation of angiotensin II and ghrelin, are important players in cardiomyocyte apoptosis. We therefore believe that microRNA-122 and Sestrin-2 can be developed as potential therapeutic targets against apoptosis in cardiovascular diseases.

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Plasma miR-122 and miR-3149 Potentially Novel Biomarkers for Acute Coronary Syndrome

Cited by 38 publications

References 30 publications

Identifying circulating microRNAs as biomarkers of cardiovascular disease: a systematic review

Identifying circulating microRNAs as biomarkers of cardiovascular disease: a systematic review

Circulating miRNA Expression Profiling and Target Prediction in Patients Receiving Dexmedetomidine

The impact of microRNA-122 and its target gene Sestrin-2 on the protective effect of ghrelin in angiotensin II-induced cardiomyocyte apoptosis

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