Emerging Roles of microRNAs in Ischemic Stroke: As Possible Therapeutic Agents

Khoshnam, Seyed Esmaeil; Winlow, William; Farbood, Yaghoob; Moghaddam, Hadi Fathi; Farzaneh, Maryam

doi:10.5853/jos.2016.01368

Cited by 136 publications

(95 citation statements)

References 249 publications

(262 reference statements)

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“…And circulating miR‐15a and miR‐16 are enriched in critical limb ischaemia (CLI) patients and serum miR‐15a expression is also positively associated with post‐revascularization restenosis 173. A recent study reported that circulating miR‐363, miR‐487b, miR‐125b‐2, miR‐27a, miR‐422a, miR‐488, miR‐627, miR‐290, miR‐10a, miR‐182, miR‐200b, miR‐298, miR‐106b‐5p and miR‐4306 are increased while circulating miR‐122, miR‐148a, let‐7i, miR‐19a, miR‐320d, miR‐4429, miR‐30a, miR‐126, miR‐9, miR‐219, miR‐320e and miR‐320d are reduced following ischaemic stroke 174. Interestingly, miR‐10a contributes to the repression of pro‐inflammatory endothelial phenotypes in atherosusceptible regions in vivo 167.…”

Section: Clinical Value Of Mirnas As New Biomarkers For Angiogenesis‐mentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

116

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MicroRNAs (miRNAs) are small non‐coding RNAs that regulate gene expression at a post‐transcriptional level via either the degradation or translational repression of a target mRNA. They play an irreplaceable role in angiogenesis by regulating the proliferation, differentiation, apoptosis, migration and tube formation of angiogenesis‐related cells, which are indispensable for multitudinous physiological and pathological processes, especially for the occurrence and development of vascular diseases. Imbalance between the regulation of miRNAs and angiogenesis may cause many diseases such as cancer, cardiovascular disease, aneurysm, Kawasaki disease, aortic dissection, phlebothrombosis and diabetic microvascular complication. Therefore, it is important to explore the essential role of miRNAs in angiogenesis, which might help to uncover new and effective therapeutic strategies for vascular diseases. This review focuses on the interactions between miRNAs and angiogenesis, and miRNA‐based biomarkers in the diagnosis, treatment and prognosis of angiogenesis‐related diseases, providing an update on the understanding of the clinical value of miRNAs in targeting angiogenesis.

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Section: Clinical Value Of Mirnas As New Biomarkers For Angiogenesis‐mentioning

confidence: 99%

The regulatory role of microRNAs in angiogenesis‐related diseases

Sun

Lei

et al. 2018

J Cellular Molecular Medi

116

View full text Add to dashboard Cite

show abstract

“…A full accounting of the potential role of miRNAs as therapeutic targets or agents for ischemic stroke is beyond the scope of our review and the reader is referred to some recent articles on the topic (Chandran et al, 2017; Gaudet et al, 2017; Kaur et al, 2018; Khoshnam et al, 2017). Rather, we focus on several miRNAs that have garnered considerable interest and are illustrative of the potential benefits and challenges of this approach.…”

Section: Recently Identified Molecular/cellular Targets and Approachesmentioning

confidence: 99%

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches

Shekhar

Cunningham

Pabbidi

et al. 2018

European Journal of Pharmacology

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Ischemic stroke is a devastating and debilitating medical condition with limited therapeutic options. However, accumulating evidence indicates a central role of inflammation in all aspects of stroke including its initiation, the progression of injury, and recovery or wound healing. A central target of inflammation is disruption of the blood brain barrier or neurovascular unit. Here we discuss recent developments in identifying potential molecular targets and immunomodulatory approaches to preserve or protect barrier function and limit infarct damage and functional impairment. These include blocking harmful inflammatory signaling in endothelial cells, microglia/macrophages, or Th17/γδ T cells with biologics, third generation epoxyeicosatrienoic acid (EET) analogs with extended half-life, and miRNA antagomirs. Complementary beneficial pathways may be enhanced by miRNA mimetics or hyperbaric oxygenation. These immunomodulatory approaches could be used to greatly expand the therapeutic window for thrombolytic treatment with tissue plasminogen activator (t-PA). Moreover, nanoparticle technology allows for the selective targeting of endothelial cells for delivery of DNA/RNA oligonucleotides and neuroprotective drugs. In addition, although likely detrimental to the progression of ischemic stroke by inducing inflammation, oxidative stress, and neuronal cell death, 20-HETE may also reduce susceptibility of onset of ischemic stroke by maintaining autoregulation of cerebral blood flow. Although the interaction between inflammation and stroke is multifaceted, a better understanding of the mechanisms behind the pro-inflammatory state at all stages will hopefully help in developing novel immunomodulatory approaches to improve mortality and functional outcome of those inflicted with ischemic stroke.

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“…Through the post‐transcriptional regulation of gene expression, miRNAs are believed to regulate various biological processes, including proliferation, apoptosis, the cell cycle, and differentiation, that are involved in both physiological and pathological progress . Currently, accumulating evidence indicates that various miRNAs are dysregulated in cerebral ischaemia/reperfusion injury and can be potentially used as diagnostic and/or therapeutic targets . Various studies demonstrated that targeting specific miRNAs can alleviate neuronal injury and recover neurological functions using in vitro and in vivo experimental models of cerebral ischaemia/reperfusion injury .…”

Section: Introductionmentioning

confidence: 99%

“…[10][11][12] Currently, accumulating evidence indicates that various miRNAs are dysregulated in cerebral ischaemia/ reperfusion injury and can be potentially used as diagnostic and/or therapeutic targets. 13,14 Various studies demonstrated that targeting specific miRNAs can alleviate neuronal injury and recover neurological functions using in vitro and in vivo experimental models of cerebral ischaemia/reperfusion injury. [15][16][17][18] However, the precise miRNA-mediated epigenetic regulatory mechanism in cerebral ischaemia/reperfusion injury remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of microRNA‐148b‐3p alleviates oxygen‐glucose deprivation/reoxygenation‐induced apoptosis and oxidative stress in HT22 hippocampal neuron via reinforcing Sestrin2/Nrf2 signalling

et al. 2020

Clin Exp Pharma Physio

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MicroRNAs (miRNAs) have emerged as crucial regulators of neuronal injury during cerebral ischaemia/reperfusion injury. Various miRNAs are dysregulated during this pathological process; however, the precise role of these miRNAs in regulating neuronal injury remains largely unknown. In the current study, we explored the potential function of microRNA‐148b‐3p (miR‐148b‐3p) in regulating neuronal injury induced by oxygen‐glucose deprivation/reoxygenation (OGD/R) in vitro, a cellular model for mimicking cerebral ischaemia/reperfusion injury. We found that miR‐148b‐3p expression was significantly decreased in neurons in response to OGD/R exposure. Importantly, miR‐148b‐3p overexpression decreased cell viability and exacerbated apoptosis and reactive oxygen species (ROS) production in OGD/R‐exposed neurons. By contrast, miR‐148b‐3p inhibition improved cell viability and decreased apoptosis and ROS production in OGD/R‐exposed neurons. Notably, Sestrin2, a cytoprotective gene, was identified as a miR‐148b‐3p target gene. miR‐148b‐3p inhibition markedly increased Sestrin2 expression as well as the activation of nuclear factor erythroid‐2‐related factor 2 (Nrf2) antioxidant signalling. Moreover, silencing of Sestrin2 or Nrf2 significantly reversed the miR‐148‐3p‐inhibition‐mediated protective effect in OGD/R‐injured neurons. Overall, these results demonstrate that miR‐148b‐3p inhibition protects neurons from OGD/R‐induced apoptosis and ROS production through reinforcing Nrf2 antioxidant signalling via upregulation of Sestrin2. Our study indicates that the miR‐148b‐3p/Sestrin2/Nrf2 axis plays an important role in regulating neuronal injury and may serve as a potential therapeutic target for providing neuroprotection during cerebral ischaemia/reperfusion injury.

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Emerging Roles of microRNAs in Ischemic Stroke: As Possible Therapeutic Agents

Cited by 136 publications

References 249 publications

The regulatory role of microRNAs in angiogenesis‐related diseases

The regulatory role of microRNAs in angiogenesis‐related diseases

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches

Inhibition of microRNA‐148b‐3p alleviates oxygen‐glucose deprivation/reoxygenation‐induced apoptosis and oxidative stress in HT22 hippocampal neuron via reinforcing Sestrin2/Nrf2 signalling

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