Non-Coding RNA in Acute Ischemic Stroke: Mechanisms, Biomarkers and Therapeutic Targets

Wang, Shengwen; Liu, Zhong; Shi, Zhong‐Song

doi:10.1177/0963689718806818

Cited by 110 publications

(82 citation statements)

References 121 publications

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“…CircRNAs have multiple regulatory functions and mechanisms that modify transcriptional and post-transcriptional regulation 7,8 . For posttranscriptional regulation, circRNAs can act as microRNA (miRNA) sponges or competitively combine with miRNA 9 . Cir-cRNAs play critical roles in various cancers.…”

Section: Introductionmentioning

confidence: 99%

Circular RNA circSLC25A16 contributes to the glycolysis of non-small-cell lung cancer through epigenetic modification

Shangguan

Hong

et al. 2020

Cell Death Dis

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Growing evidence has highlighted the roles of circular RNAs (circRNAs) in non-small-cell lung cancer (NSCLC), however, their roles in NSCLC glycolysis remains poorly understood. CircRNAs microarray profiles discovered a novel exon-derived circRNA, circSLC25A16 (hsa_circ_0018534), in NSCLC tissue samples. In NSCLC samples, high-expression of circSLC25A16 was associated with unfavorable prognosis. Cellular experiments revealed that circSLC25A16 accelerated the glycolysis and proliferation of NSCLC cells. Besides, circSLC25A16 knockdown repressed the in vivo growth by xenograft assays. RNA-fluorescence in situ hybridization (RNA-FISH) illustrated that circSLC25A16 and miR-488-3p were both located in cytoplasm. Mechanistic experiments demonstrated that circSLC25A16 interacts with miR-488-3p/HIF-1α, which activates lactate dehydrogenase A (LDHA) by facilitating its transcription. Collectively, present research reveals the crucial function of circSLC25A16 on NSCLC glycolysis through miR-488-3p/HIF-1α/LDHA, suggesting the underlying pathogenesis for NSCLC and providing a therapeutic strategy for precise treatment.

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Section: Introductionmentioning

confidence: 99%

Circular RNA circSLC25A16 contributes to the glycolysis of non-small-cell lung cancer through epigenetic modification

Shangguan

Hong

et al. 2020

Cell Death Dis

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“…Circular RNAs are a class of non‐coding RNAs that are involved in the development of vascular diseases 5,6 . Circular circTLK1 deteriorated myocardial ischaemia/reperfusion injury via regulating the TNF signalling pathway 7 .…”

Section: Introductionmentioning

confidence: 99%

Circular RNA circCCDC9 alleviates ischaemic stroke ischaemia/reperfusion injury via the Notch pathway

Zhang

et al. 2020

J Cellular Molecular Medi

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Stroke is a leading cause of mortality and disability globally. 1-3 There are more than two million ischaemic stroke cases in adults aged 18-50 years annually. 3 Modifiable lifestyle risk factors, including smoking, physical activity, diet, alcohol consumption and weight, could cut down the risk of stroke. For patients with ischaemic stroke, the most effective and frequently used treatment would be early reperfusion with intravenous thrombolysis and thrombectomy. However, these treatments are limited by a narrow time window and side effects. 4 Given this situation, there is an urgent need to develop novel treatments for patients with ischaemic stroke. Circular RNAs are a class of non-coding RNAs that are involved in the development of vascular diseases. 5,6 Circular circTLK1 deteriorated myocardial ischaemia/reperfusion injury via regulating the TNF signalling pathway. 7 CircRNAs are abundant in the brain tissues 8 and have been implicated in neurological functions 9 and acute ischaemic stroke. 6 A total of 521 differentially expressed circRNAs were found in the peripheral blood mononuclear cells of patients with acute ischaemic stroke compared to healthy controls, which suggested that circRNAs were potential markers for the diagnosis

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“…Studies have shown that several miRNAs can dramatically alter normal physiological processes and are involved in the pathogenesis of human diseases [17]. Accumulating evidence has demonstrated that aberrant expression of miRNAs play critical roles in central nervous system injury [18][19][20]. Among the miRNAs, miR-27-3p has been widely studies due to its important role in regulating in ammation and innate immune pathway [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-27a-3p Relives Inflammation and Neurologic Impairment after Cerebral Ischemia Reperfusion via Inhibiting LITAF and the TLR4/NF-κB Pathway

Luo¹,

Li²,

Li³

et al. 2020

Preprint

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Background: Cerebral ischemia reperfusion (CIR) affects microRNA (miR) expression and causes substantial inflammation. Here, we investigated the influence and underlying mechanism of miR-27-3p in rats with CIR.Methods: Cerebral ischemia reperfusion was built by tMCAO. Rats were randomly divided into Sham group, brain ischemic reperfusion (IR) group, brain ischemic reperfusion transfected with NC group, brain ischemic reperfusion transfected with miR-27a-3p mimic group, brain ischemic reperfusion transfected with miR-27a-3p inhibitor group and brain ischemic reperfusion transfected with miR-27a-3p mimic and Litaf mimic group. The relationship between miR-27a-3p and Litaf was verified via qRT-PCR and luciferase assays. The cellular distribution of Litaf was determined via double immunofluorescence. The effect of miR-27a-3p on the expression of Litaf, TLR4, NF-κB and IL-6 was evaluated using synthetic miR-27a-3p mimic and inhibitor. The level of Nissl’s body in each group was detected by Nissl’s staining. The infarct in each group was evaluated by TTC staining.Results: Firstly, BV treatment relieves cerebral infarction and decreases the levels of serum IL-1β, IL-6 and TNF-α. Through our previous study, we found key microRNA mR-27a-3p and its targeted gene Litaf might involve in the molecular mechanism of CIR. Then, the regulation between miR-27a-3p and Litaf was verified by the temporal miR-27a-3p and Litaf expression profiles and luciferase assay. Moreover, intracerebroventricular injection of the miR-27a-3p mimic significantly decreased the Litaf, TLR4, NF-κB and interleukin (IL)-6 levels and the double-labeled cell count 24 h post-surgery, whereas miR-27a-3p inhibitor reversed these effects. Furthermore, miR-27a-3p mimic could relive cerebral infarct and neurologic deficit after CIR. In addition, injection of miR-27a-3p mimic decreased neuronal damage induced by CIR.Conclusions: Increasing miR-27-3p levels protect against CIR by relieving inflammation, neuronal damage and neurologic deficit by inhibiting LITAF and the TLR4/NF-κB pathway.

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Non-Coding RNA in Acute Ischemic Stroke: Mechanisms, Biomarkers and Therapeutic Targets

Cited by 110 publications

References 121 publications

Circular RNA circSLC25A16 contributes to the glycolysis of non-small-cell lung cancer through epigenetic modification

Circular RNA circSLC25A16 contributes to the glycolysis of non-small-cell lung cancer through epigenetic modification

Circular RNA circCCDC9 alleviates ischaemic stroke ischaemia/reperfusion injury via the Notch pathway

MicroRNA-27a-3p Relives Inflammation and Neurologic Impairment after Cerebral Ischemia Reperfusion via Inhibiting LITAF and the TLR4/NF-κB Pathway

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