MicroRNA-150 aggravates H&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;O&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt;-induced cardiac myocyte injury by down-regulating &amp;lt;italic&amp;gt;c-myb&amp;lt;/italic&amp;gt; gene

Li, Xuebiao; Kong, Minjian; Jiang, Daming; Qian, Jianfang; Duan, Qun-Jun; Dong, Aiqiang

doi:10.1093/abbs/gmt067

Cited by 34 publications

(18 citation statements)

References 25 publications

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“…The upregulation of circulating miR-486 in AMI patients may be related to cardiac hypertrophy. miR-150, an miRNA related to inflammation, was reported to be implicated in the pathogenesis of various cardiovascular diseases [36–38]. A microarray screen of plasma samples showed reduced levels of miR-150 in patients with pulmonary arterial hypertension compared to healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Expression of circulating miR-486 and miR-150 in patients with acute myocardial infarction

Zhang

Lan

Peng

et al. 2015

BMC Cardiovasc Disord

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BackgroundWith its high morbidity and mortality, acute myocardial infarction (AMI) places a major burden on society and on individual patients. Correct, early correct diagnosis is crucial to the management of AMI.MethodsIn this study, the expression of circulating miR-486 and miR-150 was investigated in AMI patients and the two miRNAs were evaluated as potential biomarkers for AMI. Plasma samples from 110 patients with AMI (65 patients with ST-segment elevation myocardial infarction (STEMI) and 45 patients with non-ST-segment elevation myocardial infarction (NSTEMI)) and 110 healthy adults were collected. Circulating levels of miR-486 and miR-150 were detected using quantitative real-time PCR in plasma samples.ResultsResults showed that the levels of miR-486 and miR-150 were significantly higher in AMI patients than in healthy controls. Receiver operating characteristic (ROC) curve analyses indicated that the two plasma miRNAs were of significant diagnostic value for AMI, especially NSTEMI. The combined ROC analysis revealed an AUC value of 0.771 in discriminating AMI patients from healthy controls and an AUC value of 0.845 in discriminating NSTEMI patients from healthy controls.ConclusionResults indicated that the levels of circulating miR-486 and miR-150 are associated with AMI. They may be novel and powerful biomarkers for AMI, especially for NSTEMI.

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Section: Discussionmentioning

confidence: 99%

Expression of circulating miR-486 and miR-150 in patients with acute myocardial infarction

Zhang

Lan

Peng

et al. 2015

BMC Cardiovasc Disord

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“…Recently, dysregulated expression of miR-150 has been reported in cardiac tissues from AMI patients [25, 57], consistent with our observation that plasma miR-150-3p levels were upregulated in the AMI samples. miR-150 has been shown to aggravate H 2 O 2 -induced cardiac myocyte injury by downregulating c-Myb gene [58], a gene involved in regulating the differentiation of myogenic progenitor cells. These results suggest that miR-150 may participate in H 2 O 2 -mediated gene regulation and functional modulation in cardiac myocytes.…”

Section: Discussionmentioning

confidence: 99%

Systemic Approach to Identify Serum microRNAs as Potential Biomarkers for Acute Myocardial Infarction

Hsu

Chen

Chang

et al. 2014

BioMed Research International

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Background. Recent studies have revealed the role of microRNAs (miRNAs) in a variety of biological and pathological processes, including acute myocardial infarction (AMI). We hypothesized that ST-segment elevation myocardial infarction (STEMI) may be associated with an alteration of miRNAs and that circulating miRNAs may be used as diagnostic markers for STEMI. Methods. Expression levels of 270 serum miRNAs were analyzed in 8 STEMI patients and 8 matched healthy controls to identify miRNAs differentially expressed in the sera of patients with AMI. The differentially expressed miRNAs were evaluated in a separate cohort of 62 subjects, including 31 STEMI patients and 31 normal controls. Results. The initial profiling study identified 12 upregulated and 13 downregulated serum miRNAs in the AMI samples. A subsequent validation study confirmed that serum miR-486-3p and miR-150-3p were upregulated while miR-126-3p, miR-26a-5p, and miR-191-5p were significantly downregulated in the sera of patients with AMI. Ratios between the level of upregulated and downregulated miRNAs were also significantly different in those with AMI. Receiver operator characteristics curve analysis using the expression ratio of miR-486-3p and miR-191-5p showed an area under the curve of 0.863. Conclusion. Our results suggest that serum miRNAs may be used as potential diagnostic biomarkers for STEMI.

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“…The role of miRNAs in the regulation of cardiomyocyte apoptosis has been well documented in various studies, and these miRNAs include miR-150, miR-19a, miR-200c, miR-1 and so on [18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

The Long Non-Coding RNA SNHG1 Attenuates Cell Apoptosis by Regulating miR-195 and BCL2-Like Protein 2 in Human Cardiomyocytes

Zhang

Meng

Mei

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are theorized to play key roles in the development of heart diseases. However, the role of lncRNAs in cardiomyocyte apoptosis is largely unknown. The present study examined the role of lncRNA SNHG1 in the human cardiomyocytes (HCMs) apoptosis and explored the underlying molecular mechanisms. Methods: SNHG1, miR-195 and mRNA expression was detected by qRT-PCR; protein level was determined by western blot; cell viability was detected by MTT assay; cell apoptosis was evaluated by flow cytometry and caspase-3 activity assay; the interaction between SNHG1 and miR195 was examined by using luciferase reporter assay. Results: Hydrogen peroxide (H₂O₂) treatment significantly suppressed cell viability and increased cell apoptotic rate and caspase-3 activity in HCMs. Overexpression of SNHG1 attenuated the effects of H₂O₂ on HCMs viability and apoptosis; while SNHG1 exerted the opposite effects. SNHG1 was found to sponge miR-195 and suppress the expression of miR-195 in HCMs. Overexpression of miR-195 suppressed cell viability and induced apoptosis in HCMs, and miR-195 was found to negatively regulate the expression of BCL-2 like protein 2 (BCL2L2) via targeting its 3’ untranslated region. Overexpression of BCL2L2 partially reversed the effects of miR-195 overexpression on cell viability and cell apoptosis of HCMs. MiR-195 overexpression or BCL2L2 knockdown attenuated the effects of SNHG1 overexpression on cell viability, cell apoptosis and protein levels of cleaved caspase-3, cleaved caspase-9 and Bax in H₂O₂-treated HCMs. Conclusion: Our results suggest a novel SNHG1/miR-195/BCL2L2 axis in the regulation of cardiomyocyte apoptosis. Modulation of SNHG1 may represent a novel strategy to treat cardiomyocyte apoptosis-related heart diseases.

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MicroRNA-150 aggravates H<sub>2</sub>O<sub>2</sub>-induced cardiac myocyte injury by down-regulating <italic>c-myb</italic> gene

Cited by 34 publications

References 25 publications

Expression of circulating miR-486 and miR-150 in patients with acute myocardial infarction

Expression of circulating miR-486 and miR-150 in patients with acute myocardial infarction

Systemic Approach to Identify Serum microRNAs as Potential Biomarkers for Acute Myocardial Infarction

The Long Non-Coding RNA SNHG1 Attenuates Cell Apoptosis by Regulating miR-195 and BCL2-Like Protein 2 in Human Cardiomyocytes

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