MicroRNAs in the Blood-Brain Barrier in Hypoxic-Ischemic Brain Injury

Shen, Guofang; Ma, Qingyi

doi:10.2174/1570159x18666200429004242

Cited by 19 publications

(10 citation statements)

References 89 publications

(106 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…BBB dysfunction has been ascertained in multiple brain disorders, including stroke, traumatic brain injury (TBI), MS, epilepsy, AD, amyotrophic lateral sclerosis and PD (Daneman, 2012;Kamphuis et al, 2015). The main pathways activated upon BBB disruption consists of tight junction protein degradation, microvascular endothelial cells (ECs) damage, immune cell infiltration and activation of cytokine expression (Shen and Ma, 2020). MiRNAs have been shown to modulate BBB function under various pathological conditions, from: ischemic brain injury, TBI, spinal cord injury to neurodegenerative diseases (AD, Vascular dementia), brain tumors and cerebral infections (Ma et al, 2020).…”

Section: Blood Brain Barrier Disruptionmentioning

confidence: 99%

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

et al. 2022

View full text Add to dashboard Cite

Cerebral ischemia reperfusion injury is a debilitating medical condition, currently with only a limited amount of therapies aimed at protecting the cerebral parenchyma. Micro RNAs (miRNAs) are small, non-coding RNA molecules that via the RNA-induced silencing complex either degrade or prevent target messenger RNAs from being translated and thus, can modulate the synthesis of target proteins. In the neurological field, miRNAs have been evaluated as potential regulators in brain development processes and pathological events. Following ischemic hypoxic stress, the cellular and molecular events initiated dysregulate different miRNAs, responsible for long-terming progression and extension of neuronal damage. Because of their ability to regulate the synthesis of target proteins, miRNAs emerge as a possible therapeutic strategy in limiting the neuronal damage following a cerebral ischemic event. This review aims to summarize the recent literature evidence of the miRNAs involved in signaling and modulating cerebral ischemia-reperfusion injuries, thus pointing their potential in limiting neuronal damage and repair mechanisms. An in-depth overview of the molecular pathways involved in ischemia reperfusion injury and the involvement of specific miRNAs, could provide future perspectives in the development of neuroprotective agents targeting these specific miRNAs.

show abstract

Section: Blood Brain Barrier Disruptionmentioning

confidence: 99%

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

et al. 2022

View full text Add to dashboard Cite

show abstract

“…26,27 An increasing number of studies have shown that HI causes irreversible brain damage to the developing brain of newborns, resulting in long-term neurological deficits. [28][29][30] The hippocampus and the cortex are very sensitive to HI injury, 31 so in this study, the above regions were selected to observe the morphological changes of neurons. At 24 h after HI, the neurons of the hippocampal CA1, CA3, and cortex in the HI group showed significant morphological damage, with loss of neurons and Nissl bodies, pyknotic nuclei, and vacuolization.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Fei‐Sun

Huang

Qin

et al. 2022

Ibrain

View full text Add to dashboard Cite

Hypoxic ischemic encephalopathy (HIE) is an important cause of neonatal death and disability, which can lead to long-term neurological and motor dysfunction. At present, the treatment mainly focuses on the symptomatic treatment in the acute phase and rehabilitation after injury, but the effect is not satisfactory, and more effective methods are urgently needed. Due to the widespread use of inhalation anesthetics in surgery, it has been found that iso urane (ISO) preconditioning may have a positive effect on neuroprotection. The aim of this study was to investigate the effects of ISO preconditioning on neurological function and behavior in HIE rats. MethodsNeonatal rats were used to create hypoxic-ischemic (HI) model by ligating the right common carotid artery at 7 days and then in a hypoxia chamber. The effects of anesthetic drugs on neurological function after one hour of ISO preconditioning were assessed after modeling by Morris water maze(MWM), Ymaze, and rotarod tests at one month. Thereafter, samples were taken at 1 and 42 days for Nissl staining and Hematoxylin-Eosin (HE) staining to observe neuronal number and histomorphology changes. The relationship of behaviour and morphology tests were measured. ResultsIschemia and hypoxia could induce neuronal injury, neurological dysfunction and severe long-term motor function injury. Histological staining and behavioural evaluations were performed to elucidate the pathological changes and neurobehavioural variation after ISO treatment. We found ISO administration signi cantly reduced the infarct volume of brain tissues and improved the autonomous activities of neonatal rats, ISO preconditioning signi cantly reduced neuronal apoptosis induced by HI, reduced cerebral infarction volume, improved histopathological damage of nerve cells, improved long-term cognitive function, and attenuated HI-induced Nissl total cells to reduce and reduce long-term spatial memory impairment caused by hypoxia-ischemia during the maturation of injured brain. ConclusionISO preconditioning can protect the brain injury and promote the recovery of neurological function in neonatal rats with HIE, which may be through inhibiting the neuronal cell death in the cortex and hippocampus after HI.

show abstract

“…Hypoxic-ischemic brain damage (HIBD) is structural damage and dysfunction caused by lack or limitation of oxygen and glucose supply in the human brain, and long-term ischemia can lead to severe or fatal damage to the brain [1,2]. HIBD is one of the leading causes of chronic disability and acute mortality in neonates [3,4]. The treatment of HIBD mainly depends on ibuprofen, stem cell therapy, hypothermia therapy, neuroprotective agents and combination therapy, whereas, up to now, the specific measures and standards for its treatment are imperfect [3].…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine alleviates the hypoxic-ischemic brain damage via miR-20a-5p/methionine adenosyltransferase 2B axis in rat pups

Sun²,

Chen³

et al. 2022

NeuroReport

View full text Add to dashboard Cite

Objective The neuroprotective effect of dexmedetomidine (DEX) has been demonstrated in hypoxic-ischemic brain damage (HIBD) animal models, the mechanism of which will be the foothold in this work. Methods After establishment of HIBD rat model, the rats were treated with DEX, miR-20a-5p agomir and adenoviral methionine adenosyltransferase 2B (MAT2B) overexpression vector, and then their brain tissues were harvested. The infarction volume and pathological changes of these brain tissues were measured using the triphenyl tetrazolium chloride (TTC), Nissl and hematoxylin–eosin (HE) stainings. The levels of miR-20a-5p, Bcl-2, Bax and MAT2B in these brain tissues were detected by Real-Time PCR (RT-PCR) and western blot. The binding sites of MAT2B and miR-20a-5p were predicted using the TargetScan and verified using the dual-luciferase reporter assay. The memory deficits and spatial learning of rat pups were assessed by Morris water maze test. Results MiR-20a-5p expression was upregulated, while MAT2B expression was downregulated in rats with HIBD. MAT2B was targeted by miR-20a-5p. DEX treatment improved the neurons and hippocampal tissue damage and decreased miR-20a-5p level in brain tissues of rats with HIBD. MiR-20a-5p overexpression overturned the protective effect of DEX on brain tissues and learning and memory abilities in rats with HIBD. Moreover, DEX promoted Bcl-2 level while inhibiting Bax level in HIBD rats’ brain tissues. Besides, overexpressed MAT2B reversed the effect of overexpressed miR-20a-5p on the levels of MAT2B, Bcl-2 and Bax, brain tissue damage, as well as the learning and memory abilities in rats with HIBD. Conclusion DEX alleviated HIBD via the miR-20a-5p/MAT2B axis in rats.

show abstract

MicroRNAs in the Blood-Brain Barrier in Hypoxic-Ischemic Brain Injury

Cited by 19 publications

References 89 publications

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

Protective effect of isoflurane preconditioning on neurological function in rats with HIE

Dexmedetomidine alleviates the hypoxic-ischemic brain damage via miR-20a-5p/methionine adenosyltransferase 2B axis in rat pups

Contact Info

Product

Resources

About