Synergy of circulating miR-212 with markers for cardiovascular risks to enhance estimation of atherosclerosis presence

Jeong, Hye Seon; Kim, Jee-Yeon; Lee, Seo Hyun; Hwang, Junha; Shin, Jong Wook; Song, Kyu Sang; Lee, Sukhoon; Kim, Jei

doi:10.1371/journal.pone.0177809

Cited by 17 publications

(15 citation statements)

References 48 publications

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“…The dysregulation of various miRNAs in atherosclerosis has been widely reported [7,9,15]. Our study results show an elevated serum miR-186-5p level in atherosclerosis patients, meaning that miR-186-5p might have a function in its occurrence and pathogenesis.…”

Section: Discussionsupporting

confidence: 56%

“…MicroRNAs (miRNAs) affect various biological processes by regulating target mRNA expression [5]. MiRNA dysregulation occurs in multiple human diseases, including atherosclerosis [6,7], and the clinical values of these aberrantly expressed miRNAs are leveraged in the diagnosis and prognosis of human diseases [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…MiR-29b overexpression is detected in the serum of atherosclerosis patients, and its expression level is positively associated with carotid intima-media thickness (CIMT) of patients [9]. Another study by Jeong et al found that the serum miR-212 level shows a significant increase in atherosclerosis patients and identified circulating miR-212 as a novel marker of atherosclerosis [7]. The plasma miR-186-5p level is also aberrant in the early stage of acute myocardial infarction (AMI) and there is an evident correlation between the occurrence of AMI and the presence of atherosclerosis [10,11].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-186-5p serves as a diagnostic biomarker in atherosclerosis and regulates vascular smooth muscle cell proliferation and migration

et al. 2020

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Objective: MicroRNA dysregulation occurs in many human diseases, including atherosclerosis. Here, we examined the serum expression and clinical significance of miR-186-5p in patients with atherosclerosis, and explored its influence on vascular smooth muscle cell (VSMC) proliferation and migration. Methods: Blood samples were collected from 104 patients with asymptomatic atherosclerosis and 80 healthy controls. Quantitative real-time PCR was applied to measure the miR-186-5p level. An ROC curve was established to assess the discriminatory ability of the serum miR-186-5p level for identifying atherosclerosis from controls. CCK-8 and Transwell assays were used to evaluate the impact of miR-186-5p on cell behaviors. Results: Serum expression of miR-186-5p was significantly higher in atherosclerosis patients than in the control group. The serum miR-186-5p level showed a positive correlation with CIMT and could be used to distinguish atherosclerosis patients from healthy controls, with an area under the curve (AUC) score of 0.891. In VSMCs, overexpression of miR-186-5p significantly promoted cell proliferation and migration, while the opposite results were observed when miR-186-5p was downregulated. Conclusion: Overexpression of miR-186-5p has a certain diagnostic significance for atherosclerosis. Upregulation of miR-186-5p stimulates VSMC proliferation and migration. Therefore, it is a possible target for atherosclerosis interventions.

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA-186-5p serves as a diagnostic biomarker in atherosclerosis and regulates vascular smooth muscle cell proliferation and migration

et al. 2020

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“…A recent study reported by Kumarswamy et al (), acknowledged the contribution of miR‐212 to endothelial vasodilatory function and angiogenic responses in adult mice. Furthermore, Jeong et al () noted that miR‐212 could work as a novel atherosclerosis estimation marker in ischemic stroke patients. Considering the various potential targets governed by each miRNA, the persistent challenge of understanding functional miRNA contributions in disease cell behaviors depends on the identification of bona fide molecular targets.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐212 promotes the recovery function and vascular regeneration of endothelial progenitor cells in mice with ischemic stroke through inactivation of the notch signaling pathway via downregulating MMP9 expression

Dong

2018

Journal Cellular Physiology

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Ischemic stroke is a refractory disease caused by cerebral ischemic injury, which results in brain dysfunction. This study intends to investigate the effects of microRNA-212 (miR-212) on the recovery function and vascular regeneration of endothelial progenitor cells (EPCs) by inactivation of the Notch signaling pathway by binding to matrix metallopeptidase 9 (MMP9) in mice with ischemic stroke. According to the results of database retrieval systems and data analysis, MMP9 was predicted as a gene related to ischemic stroke and miR-212 is a potential regulating mRNA of MMP9. All 72 healthy adult C57BL6 mice were selected for middle cerebral artery occlusion (MCAO) establishment. Cerebral infarction was observed under triphenyltetrazolium chloride staining. A series of inhibitors, activators, and siRNAs were introduced to the verified regulatory functions for miR-212 governing MMP9 in ischemic stroke. Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and tube-forming ability by tubule formation test. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were used to detect the expressions of miR-212, MMP9, Hes-1, and Notch-1. The corresponding results demonstrated that the area of cerebral infarction and the number of neuronal necrosis increased in the MCAO group in contrast to the sham group. Meanwhile, upregulation of miR-212 or downregulation of MMP9 decreases the expressions of MMP9, Hes-1 Notch-1, increases cell proliferation and tube-forming ability and improves the pathological conditions of EPCs. Our study suggests that miR-212 promotes recovery function and vascular regeneration of EPCs through negative regulation of the Notch signaling pathway via downregulating expression of MMP9, thus provides a clinical theoretical basis for ischemic stroke therapy. K E Y W O R D S endothelial progenitor cells (EPCs), ischemic stroke, metallopeptidase 9 (MMP9), microRNA-212, notch pathway, vascular regeneration J Cell Physiol. 2019;234:7090-7103. wileyonlinelibrary.com/journal/jcp 7090 |

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“…MiR-212, located on chromosome 17p13.3, is deregulated in several human cancers [6, 7]. MiR-212 suppresses tumors in non-small cell lung cancer and gastric carcinoma [8].…”

Section: Introductionmentioning

confidence: 99%

MiR-212-5p Suppresses the Epithelial-Mesenchymal Transition in Triple-Negative Breast Cancer by Targeting Prrx2

Yang

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype. Our study investigated the functional role of miR-212-5p in TNBC. Methods: Realtime PCR was used to quantify miR-212-5p expression levels in 30 paired TNBC samples and adjacent normal tissues. Wound healing and Transwell assays were used to evaluate the effects of miR-212-5p expression on the invasiveness of TNBC cells. Luciferase reporter and Western blot assays were used to verify whether the mRNA encoding Prrx2 is a major target of miR-212-5p. Results: MiR-212-5p was downregulated in TNBC, and its expression levels were related to tumor size, lymph node status and vascular invasion in breast cancer. We also observed that the miR-212-5p expression level was significantly correlated with a better prognosis in TNBC. Ectopic expression of miR-212-5p induced upregulation of E-cadherin expression and downregulation of vimentin expression. The expression of miR212-5p also suppressed the migration and invasion capacity of mesenchymal-like cancer cells accompanied by a morphological shift towards the epithelial phenotype. Moreover, our study observed that miR-212-5p overexpression significantly suppressed Prrx2 by targeting its 3’-untranslated region (3’-UTR) region, and Prrx2 overexpression partially abrogated miR-212-5p-mediated suppression. Conclusions: Our study demonstrated that miR-212-5p inhibits TNBC from acquiring the EMT phenotype by downregulating Prrx2, thereby inhibiting cell migration and invasion during cancer progression.

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Synergy of circulating miR-212 with markers for cardiovascular risks to enhance estimation of atherosclerosis presence

Cited by 17 publications

References 48 publications

MicroRNA-186-5p serves as a diagnostic biomarker in atherosclerosis and regulates vascular smooth muscle cell proliferation and migration

MicroRNA-186-5p serves as a diagnostic biomarker in atherosclerosis and regulates vascular smooth muscle cell proliferation and migration

MicroRNA‐212 promotes the recovery function and vascular regeneration of endothelial progenitor cells in mice with ischemic stroke through inactivation of the notch signaling pathway via downregulating MMP9 expression

MiR-212-5p Suppresses the Epithelial-Mesenchymal Transition in Triple-Negative Breast Cancer by Targeting Prrx2

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