Exploring the potential value of miR-148b-3p, miR-151b and miR-27b-3p as biomarkers in acute ischemic stroke

Cheng, Xian; Kan, Pengcheng; Ma, Zhuolin; Wang, Yaru; Song, Wen; Huang, Chao; Zhang, Biao

doi:10.1042/bsr20181033

Cited by 36 publications

(29 citation statements)

References 17 publications

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“…The in vitro OGD/R SH-SY5Y model showed IGFBP3 was significantly decreased, which was opposite with miR-19a-3p expression. In agreement with our findings, decreased IGFBP3 expression was negatively correlated with miR-27-3p level in blood samples drawn from ischemic stroke patients [36]. Moreover, lower plasma concentration of IGF-1/IGFBP3 increased the risk of prevalent and incident dementia [37].…”

Section: Discussionsupporting

confidence: 91%

Inhibition of miR-19a-3p decreases cerebral ischemia/reperfusion injury by targeting IGFBP3 in vivo and in vitro

et al. 2020

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Background: Inflammation and apoptosis are considered to be two main factors affecting ischemic brain injury and the subsequent reperfusion damage. MiR-19a-3p has been reported to be a possible novel biomarker in ischemic stroke. However, the function and molecular mechanisms of miR-19a-3p remain unclear in cerebral ischemia/reperfusion (I/R) injury. Methods: The I/R injury model was established in vivo by middle cerebral artery occlusion/reperfusion (MCAO/R) in rats and in vitro by oxygen-glucose deprivation and reperfusion (OGD/R) induced SH-SY5Y cells. The expression of miR-19a-3p was determined by reverse transcription quantitative PCR. The infarction volumes, Neurological deficit scores, apoptosis, cell viability, pro-inflammatory cytokines and apoptosis were evaluated using Longa score, Bederson score, TTC, TUNEL staining, CCK-8, ELISA, flow cytometry assays. Luciferase reporter assay was utilized to validate the target gene of miR-19a-3p. Results: We first found miR-19a-3p was significantly up-regulated in rat I/R brain tissues and OGD/R induced SH-SY5Y cells. Using the in vivo and in vitro I/R injury model, we further demonstrated that miR-19a-3p inhibitor exerted protective role against injury to cerebral I/R, which was reflected by reduced infarct volume, improved neurological outcomes, increased cell viability, inhibited inflammation and apoptosis. Mechanistically, miR-19a-3p binds to 3′UTR region of IGFBP3 mRNA. Inhibition of miR-19a-3p caused the increased expression of IGFBP3 in OGD/R induced SH-SY5Y cells. Furthermore, we showed that IGFBP3 overexpression imitated, while knockdown reversed the protective effects of miR-19a-3p inhibitor against OGD/R-induced injury. Conclusions: In summary, our findings showed miR-19a-3p regulated I/R-induced inflammation and apoptosis through targeting IGFBP3, which might provide a potential therapeutic target for cerebral I/R injury.

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Section: Discussionsupporting

confidence: 91%

Inhibition of miR-19a-3p decreases cerebral ischemia/reperfusion injury by targeting IGFBP3 in vivo and in vitro

et al. 2020

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“…A number of reports have previously demonstrated that circulating serum miRNAs may serve as potential non-invasive biomarkers for patients with AIS (5,29). For instance, Wang et al (29) reported that serum miR-497 expression was significantly enhanced in patients with AIS compared with healthy controls.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, Wang et al (29) reported that serum miR-497 expression was significantly enhanced in patients with AIS compared with healthy controls. Cheng et al (5) suggested that miR-148b-3p, miR-151b and miR-27b-3p may serve as potential biomarkers for diagnosing AIS, with the specific combination of miR-148b-3p and miR-27b-3p being more effective. In accordance with these previous observations, the levels of serum miR-135 in patients with AIS were analyzed based on etiology.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to having 6.1% mortality, stroke is also associated with a high risk of disability and recurrence around the world, accounting for 3% of the total health expenditure (2)(3)(4). This condition is mainly divided into two categories, ischemic stroke and hemorrhagic stroke, of which the former is the most prevalent, accounting for ~80% of total cases (5). Common risk factors for this disease include high blood pressure, smoking, hyperlipidemia, obesity, diabetes, coronary heart disease and a family history of stroke (6).…”

Section: Introductionmentioning

confidence: 99%

“…In recent years, studies have demonstrated that microRNAs (miRs/miRNAs) serve important roles in a number of diseases, including vascular disease, metabolic disease and cancer (8,9). Recent studies showed that miRNAs can potentially serve as novel biomarkers and therapeutic targets for a variety of pathological conditions (5). miRNAs have a wide range of biological functions and remain stable in bodily fluids including blood, urine and amniotic fluid (10,11).…”

Section: Introductionmentioning

confidence: 99%

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miR-135b levels in the peripheral blood serve as a marker associated with acute ischemic stroke

Yang

Wang³

et al. 2020

Exp Ther Med

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The protective role of microRNA (miR)-135b in cerebral neurons has been previously identified. However, to the best of our knowledge, the involvement of miR-135b in acute ischemic stroke has yet to be elucidated. The present study aimed to investigate the expression profile of miR-135b in peripheral blood obtained from patients with acute ischemic stroke. A total of 76 patients with acute ischemic stroke were selected as the case group, which included 33 cases of aorta atheromatous plague, 19 cases of cardioembolism, 16 cases of small arterial occlusion and 8 cases with unknown causes. In addition, 60 healthy subjects were selected as the control group. Reverse transcription-quantitative PCR was used to measure the expression of miR-135b in the peripheral blood of the patients. The National Institutes of Health Stroke Scale (NIHSS) score was used to evaluate the severity of acute ischemic stroke. The relationship between miR-135b levels and acute stroke was subsequently analyzed. The expression of miR-135b in the peripheral blood of the case group was found to be significantly higher compared with that in the control group. By contrast, the expression levels of miR-135b in the case group did not differ significantly between the different etiology types of acute ischemic stroke. In addition, a significant positive correlation was observed between levels of miR-135b expression and NIHSS scores. Further analysis demonstrated that hypertension, hyperglycemia, platelet count, international normalized ratio and miR-135b were risk factors for acute ischemic stroke. Based on bioinformatics analysis, a conserved binding site for miR-135b was identified in the 3'-untranslated region of the transient receptor potential cation channel subfamily C member 6 (TRPC6). Dual luciferase reporter and western blot analysis showed that TRPC6 was a target gene of miR-135b. In conclusion, data from the present study suggest that elevated expression of miR-135b in the peripheral blood of patients with acute ischemic stroke is closely associated with disease severity.

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Research progress of IGF‐1 and cerebral ischemia

Zhou

et al. 2021

Ibrain

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Cerebral ischemic disease is a group of diseases that cause insufficient blood supply to the cerebrum, cerebellum or brain stem for different reasons, resulting in corresponding nervous system symptoms. Cardiovascular disease is the leading cause of death in the world. Among them, the death caused by cerebral ischemia accounts for the vast majority, and it is one of the fatal diseases in the middle‐aged and elderly at present. Epidemiologic studies have projected increasing mortality due to cardiovascular disease worldwide (about 23.3 million people by 2030) because of the aging population. However, related studies have shown that insulin‐like growth factor I (IGF‐1) is a multifunctional cell proliferation regulator. It plays an important role in cerebral ischemia. It is effective in promoting cell differentiation, proliferation and individual development. Studies have shown that IGF‐1 signaling pathway is a key pathway controlling cell growth and survival. There may be five mechanisms in cerebral ischemia: prevention of intracellular calcium overload, inhibition of the upregulation of nNOS, IGF‐1upregulations activating HIF‐1α, regulation of Bcl‐2 to resist apoptosis, and enhancement of vascular endothelial function. Three critical nodes in the IGF‐1 signaling pathway have been described in cardiomyocytes: protein kinase Akt/mammalian target of rapamycin (mTOR), Ras/Raf/extracellular signal‐regulated kinase (ERK), and phospholipase C (PLC)/inositol 1,4,5‐triphosphate (InsP3)/Ca2+. IGF‐1 plays an important role in cerebral ischemia and myocardial ischemia, mainly by activating downstream of IGF‐1, controlling cell death and differentiation or transcription work, improving the function of heart muscle cells, reducing the myocardial cell apoptosis induced by myocardial infarction, regulating endogenous protection and restoration of cerebral ischemia injury, thus protecting cerebral and myocardial injury. Related studies have shown that bcl‐2 exerts great influence on both cerebral ischemia and myocardial ischemia. Therefore, the relevant pathways and targets of cerebral ischemia and myocardial ischemia and the role of IGF‐1 in protecting the heart are reviewed in this paper.

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Exploring the potential value of miR-148b-3p, miR-151b and miR-27b-3p as biomarkers in acute ischemic stroke

Cited by 36 publications

References 17 publications

Inhibition of miR-19a-3p decreases cerebral ischemia/reperfusion injury by targeting IGFBP3 in vivo and in vitro

Inhibition of miR-19a-3p decreases cerebral ischemia/reperfusion injury by targeting IGFBP3 in vivo and in vitro

miR-135b levels in the peripheral blood serve as a marker associated with acute ischemic stroke

Research progress of IGF‐1 and cerebral ischemia

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