Noncoding RNAs in ischemic stroke: time to translate

Kaur, Harpreet; Sarmah, Deepaneeta; Saraf, Jackson; Vats, Kanchan; Kalia, Kiran; Borah, Anupom; Yavagal, Dileep R.; Dave, Kunjan R.; Ghosh, Zhumur; Bhattacharya, Pallab

doi:10.1111/nyas.13612

Cited by 43 publications

(29 citation statements)

References 165 publications

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“…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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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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“…Stroke leads to the induction of inflammatory cascade via migration of activated microglia to the ischemic core, worsening its outcomes (Perera et al, ). The narrow therapeutic window and insufficiency to recover or protect the dying neurons are certain limitations of current treatment strategies for stroke, so there is an urgent need for an alternative approach (Fann et al, ; Kaur et al, ). The limitation to improve the aggravated inflammatory condition by currently used thrombolytic agents necessitates newer treatment options for stroke (Carroll, ).…”

Section: Strokementioning

confidence: 99%

Therapeutic spectrum of interferon‐β in ischemic stroke

Wanve

Kaur

Sarmah

et al. 2018

J of Neuroscience Research

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Ischemic stroke is devastating and a major cause of morbidity and mortality worldwide. To date, only clot retrieval devices and/or intravenous tissue plasminogen activators (tPA) have been approved by the US-FDA for the treatment of acute ischemic stroke. Therefore, there is an urgent need to develop an effective treatment for stroke that can have limited shortcomings and broad spectrum of applications.Interferon-beta (IFN-β), an endogenous cytokine and a key anti-inflammatory agent, contributes toward obviating deleterious stroke outcomes. Therefore, exploring the role of IFN-β may be a promising alternative approach for stroke intervention in the future. In the present review, we have discussed about IFN-β along with its different mechanistic roles in ischemic stroke. Furthermore, therapeutic approaches targeting the inflammatory cascade with IFN-β therapy that may be helpful in improving stroke outcome are also discussed. K E Y W O R D S Anti-inflammatory, cytokines, IFNβ, stroke | 117 WANVE et al. How to cite this article: Wanve M, Kaur H, Sarmah D, et al. Therapeutic spectrum of interferon-β in ischemic stroke.

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“…Ischemic stroke is a refractory disease with a high incidence, high rate of disability and high mortality [1]. Due to the narrow therapeutic window and insufficiency of neuroprotective treatment for dying neurons [2,3], alternative approaches are urgently needed. Recent years have witnessed great progress in the development of neuroprotective drugs, such as edaravone, a free radical scavenger, argatroban, a direct thrombin inhibitor, butylphthalide, a mitochondrial protective agent and bradykinin receptor agonists of tissue kallikrein (TK).…”

Section: Introductionmentioning

confidence: 99%

The Mechanism of Ischemic Preconditioning Up-Regulation the Expression of Tissue Kallikrein Protects Neurons from Cerebral Ischemia/Reperfusion Injury

Shunhua

Liang

Kuang

et al. 2020

Preprint

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Ischemic stroke is an important clinical problem with few effective treatments. Many studies have shown that exogenous tissue kallikrein (TK) can protect neurons against hypoxia/reoxygenation injury. In the present study, we explored the possible molecular mechanisms underlying the regulation and function of endogenous TK. Western blot, chromatin immunoprecipitation (ChIP) and real-time PCR (RT-PCR) revealed that cerebral ischemic preconditioning (IP) upregulated the expression of endogenous TK by regulating the acetylation of histone H3. Cresyl violet staining was used to assess the neuroprotective role of endogenous TK on rat hippocampal CA1 neurons against cerebral ischemia/reperfusion (I/R) injury. Western blot results showed that IP activated the expression of p-Raf, p-MEK1/2 and p-ERK1/2 by Western blot. Moreover, Western blotfurther determined that endogenous TK upregulated the expression of p-Bad, depressed the release of cytochrome c and Bax from mitochondria to the cytosol and inhibited caspase-3 activation. In conclusion, endogenous TK can play a neuroprotective role and its upregulation induced by IP treatment can activate the phosphorylation of Raf, MEK1/2 and p-ERK1/2, depress the release of cytochrome c and Bax from mitochondria to the cytosol and inhibit caspase-3 activation.

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Noncoding RNAs in ischemic stroke: time to translate

Cited by 43 publications

References 165 publications

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

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

Therapeutic spectrum of interferon‐β in ischemic stroke

The Mechanism of Ischemic Preconditioning Up-Regulation the Expression of Tissue Kallikrein Protects Neurons from Cerebral Ischemia/Reperfusion Injury

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