Circulating MicroRNAs as Biomarkers for Acute Ischemic Stroke: A Systematic Review

Dewdney, Brittany; Trollope, Alex; Moxon, Joseph V.; Manapurathe, Diana Thomas; Biroš, Erik; Golledge, Jonathan

doi:10.1016/j.jstrokecerebrovasdis.2017.09.058

Cited by 71 publications

(51 citation statements)

References 19 publications

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“…These discoveries have initiated the novel strategy of using peripheral blood miRNAs for non-invasive disease diagnosis (4). Research reported that peripheral blood miRNAs with specific expression changes can be found in multiple diseases, including tumor, diabetes, myocardial infarction, Parkinson' disease and Alzheimer's disease (11). In the present study, overexpression of miR-323 was found to significantly increase LDH activity level and inhibit cell viability in an in vitro model of ACI.…”

Section: Discussionsupporting

confidence: 55%

“…Certain miRNAs serve important roles in neurogenesis and neuronal function, even at low concentrations. The majority of miRNAs are located in the tissues and cells (11), while they can also stably exist in body fluids, including blood, urine and amniotic fluid (12). Human tissue miRNA detection can hardly be achieved or repeatedly used in clinical practice.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-323 suppresses nerve cell toxicity in cerebral infarction via the transforming growth factor-β1/SMAD3 signaling pathway

Che

Wei

et al. 2018

Int J Mol Med

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In the present study, the aim was to investigate the function of microRNA-323 (miR-323) in cerebral infarction and its underlying mechanism. A rat model of cerebral infarction was established and hippocampal tissues were analyzed. In addition, to further understand the role of miR-323, PC12 cells were transfected with miR-323 mimics or inhibitors and subjected to hypoxia to model cerebral infarction. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression of miR-323. A luciferase reporter assay was conducted to analyze miR-323 target sites the partial sequence of the 3'-untranslated region of SMAD3 mRNA in vitro. Western blot analysis was also used to analyze transforming growth factor-β1 (TGF-β1) and SMAD3 protein expression levels. It was observed that miR-323 expression was significantly upregulated in rats with cerebral infarction compared with rats in the sham-control group. In addition, overexpression of miR-323 induced nerve cell toxicity and reduced nerve cell growth in an in vitro model of cerebral infarction, whereas downregulation of miR-323 caused the opposite effects on nerve cell toxicity and growth in this model. In addition, overexpression of miR-323 directly targeted and suppressed SMAD3 expression in the in vitro model of cerebral infarction, while inhibition of miR-323 induced SMAD3 expression. The use of a SMAD3 inhibitor suppressed the effect of anti-miR-323 on nerve cell toxicity in the in vitro model of cerebral infarction. Collectively, these findings suggested that miR-323 suppresses nerve cell apoptosis in cerebral infarction via the TGF-β1/SMAD3 signaling pathway.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

MicroRNA-323 suppresses nerve cell toxicity in cerebral infarction via the transforming growth factor-β1/SMAD3 signaling pathway

Che

Wei

et al. 2018

Int J Mol Med

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“…Over the past decade, many studies have demonstrated that miRNAs are associated with the occurrence and development of various diseases (Lu et al, 2005;Liu et al, 2010;Li and He 2012;Di Gregoli et al, 2017). Some recent studies have demonstrated that the expression patterns of miRNAs are altered in patients with various neurological disorders, including ischemic stroke (Tan et al, 2009;Dewdney et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

miRNA-223-3p and let-7b-3p as potential blood biomarkers associated with the ischemic penumbra in rats

Li¹,

Chen²,

Zhou³

et al. 2019

Acta Neurobiologiae Experimentalis

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The present study aimed to identify commonalities in the microRNA (miRNA) expression profiles of the brain ischemic penumbra and the blood after hyperacute ischemic stroke and then to address whether the miRNA profile of blood has potential usefulness as a diagnostic biomarker of hyperacute ischemic stroke. Blood was collected from the jugular vein 4 h after permanent middle cerebral artery occlusion (pMCAO). After venous blood was collected, the rats were decapitated immediately, and brain ischemic penumbra samples were collected. Hematoxylin and eosin staining was used to observe the histopathological changes. Penumbra and blood miRNAs were measured by miRNA microarray and real-time polymerase chain reaction (PCR) analysis. MicroRNA profiles differed between hyperacute ischemic stroke and sham-operated rats. The expression of some miRNAs changed by more than 1.5-fold in the penumbra and blood 4 h after pMCAO; among those miRNAs, several were upregulated and several were downregulated. MiR-223-3p was found to be highly expressed in both the penumbra and the blood 4 h after pMCAO, and let-7b-3p was found to have low expression in both the penumbra and the blood 4 h after pMCAO. Moreover, miR-223-3p and let-7b-3p expression in blood and brain ischemic penumbra were positively correlated. The results show that select blood miRNAs may correlate with miRNA changes in the penumbra in a rat model of hyperacute ischemic stroke. Our findings suggest the potential usefulness of blood miR-223-3p and let-7b-3p as noninvasive biomarkers for the diagnosis of hyperacute ischemic stroke.

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“…Increasing attention has been given to secreting miRNAs. Circulating miRNAs have been reported as novel diagnostic or therapeutic targets in several human diseases, based on the analysis of miRNAs isolated from the plasma of patients [20,21,22]. However, the use of plasma miRNAs faces technical limitations because of the extremely low concentrations of miRNAs freely circulating in the plasma, leaving the underlying molecular mechanisms regulated by miRNAs poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-Regulated miRNAs in Human Mesenchymal Stem Cells: Exploring the Regulatory Effects in Ischemic Disorders

Dell’Aversana

Cuomo

Botti

et al. 2019

IJMS

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Human mesenchymal/stromal stem cells (hMSC) are the most promising cell source for adult cell therapies in regenerative medicine. Many clinical trials have reported the use of autologous transplantation of hMSCs in several disorders, but with limited results. To exert their potential, hMSCs could exhibit efficient homing and migration toward lesion sites among other effects, but the underlying process is not clear enough. To further increase the knowledge, we studied the co-regulation between hypoxia-regulated genes and miRNAs. To this end, we investigated the miRNA expression profile of healthy hMSCs in low oxygen/nutrient conditions to mimic ischemia and compared with cells of patients suffering from critical limb ischemia (CLI). miRNAs are small, highly conserved, non-coding RNAs, skilled in the control of the target’s expression level in a fine-tuned way. After analyzing the miRNOme in CLI-derived hMSC cells and healthy controls, and intersecting the results with the mRNA expression dataset under hypoxic conditions, we identified two miRNAs potentially relevant to the disease: miR-29b as a pathological marker of the disease and miR-638 as a therapeutic target. This study yielded a deeper understanding of stem cell biology and ischemic disorders, opening new potential treatments in the future.

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Circulating MicroRNAs as Biomarkers for Acute Ischemic Stroke: A Systematic Review

Cited by 71 publications

References 19 publications

MicroRNA-323 suppresses nerve cell toxicity in cerebral infarction via the transforming growth factor-β1/SMAD3 signaling pathway

MicroRNA-323 suppresses nerve cell toxicity in cerebral infarction via the transforming growth factor-β1/SMAD3 signaling pathway

miRNA-223-3p and let-7b-3p as potential blood biomarkers associated with the ischemic penumbra in rats

Hypoxia-Regulated miRNAs in Human Mesenchymal Stem Cells: Exploring the Regulatory Effects in Ischemic Disorders

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