Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

Sun, Liqun; Guo, Guimei; Zhang, Sai; Yang, Lili

doi:10.1159/000486923

Cited by 22 publications

(15 citation statements)

References 45 publications

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“…Tert-butylhydroquinone post-treatment inhibited apoptosis and neuronal degeneration, suppressed inflammatory cytokines, and abated oxidative stress in the cerebral cortex of neonatal rat [32]. miR-592-5p overexpression decreased the apoptosis rate of hippocampal neuronal cells and protected against HI brain injuryinduced hippocampal neuronal injury [33]. Until now, finding effective therapeutic method is still urgent and important for reducing the mortality of neonates.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

Zhao

Jian

et al. 2018

Cell Cycle

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Objective: To investigate the underlying mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in hypoxic-ischemic (HI)-induced neonatal cerebral palsy. Materials and methods: Neonatal rat model of HI injury was established to detect the motor function. LncRNA MIAT, miR-211, glial cell line-derived neurotrophic factor (GDNF) and caspase-3 expressions were measured by qRT-PCR or western blot. The apoptosis of Neuro2A cells was detected by flow cytometry. RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the interaction between MIAT and miR-211. Results: Compared with control group, lncRNA MIAT and GDNF were downregulated in striatal tissues of neonatal rats in HI group and oxygen glucose deprivation (OGD)-induced ischemic injury of Neuro2A cells, whereas miR-211 was up-regulated in striatal tissues of HI group and OGDinduced ischemic injury of Neuro2A cells. LncRNA MIAT interacted with miR-211, and lncRNA MIAT overexpression reduced neuron apoptosis through miR-211. Besides, GDNF expression was positively regulated by lncRNA MIAT and negatively regulated by miR-211 in Neuro2A cells. In vivo experiment proved MIAT promoted motor function and relieved HI injury. Conclusion: MIAT overexpression reduced apoptosis of Neuro2A cells through miR-211/GDNF, which relieved HI injury of neonatal rats.

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Section: Discussionmentioning

confidence: 99%

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

Zhao

Jian

et al. 2018

Cell Cycle

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“…The mouse primary hippocampal neurons were subjected to OGD as follows: after 5-day culture, the primary neuronal cells with 90% confluence were collected after centrifugation, and then maintained with Earle balanced salt solution (HyClone) in an incubator containing 5% O 2 and 95% N 2 at 37°C for 2 hours 25. The supernatant was collected for the treatment of primary microglia.…”

Section: Methodsmentioning

confidence: 99%

Effects of hydrogen on polarization of macrophages and microglia in a stroke model

Ning¹,

Liu²,

Huang³

et al. 2018

Med Gas Res

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It has been confirmed that inflammation plays an important role in the pathogenesis of ischemic stroke. The polarization of microglia as an important participant in the inflammation following stroke is also found to be involved in stroke. This study aimed to investigate the effects of hydrogen gas on the polarization of macrophages/microglia in vitro. Raw264.7 cells were treated with lipopolysaccharides and then exposed to hydrogen. The microglia were treated with the supernatant from oxygen and glucose deprivation-treated neurons and then exposed to hydrogen. The phenotypes of Raw 264.7 cells and microglia were determined by flow cytometry, and cell morphology was observed. Results showed lipopolysaccharides significantly increased the M1 macrophages, and the supernatant from oxygen and glucose deprivation-treated neurons dramatically elevated the proportion of M1 microglia, but both treatments had little influence on the M2 cells. In addition, hydrogen treatment significantly inhibited the increase in M1 cells, but had no influence on M2 ones. Our findings suggest that the neuroprotection of hydrogen may be related to its regulation of microglia in the nervous system after stroke.

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“…Let-7b released from neurons and immune cells following injury exacerbates neuronal cell death and induces neuroinflammation (Lehmann et al, 2012; Mueller et al, 2014). The downregulation of miR-592 following hypoxic-ischemic injury induces apoptosis in hippocampal neurons (Sun et al, 2018).…”

Section: Mirnas In Cns Developmentmentioning

confidence: 99%

“…miR-29c (Yi Zhang et al, 2015) and miR-17-92 cluster (Zhang et al, 2013) attenuates the inhibitory effect of chondroitin sulphate proteoglycans (CSPG) on axonal regrowth by stimulating ras homolog family member A (RhoA) and phosphate and tensin homolog (PTEN) protein levels. miR-592 attenuates the activation of pro-apoptotic signalling and neuronal death by targeting the prostaglandin D2 receptor (PTGDR) and neurotrophin receptor (NTR) p75 (Irmady et al, 2014; Sun et al, 2018). In-vivo evidence: miR-27a reduces TLR4-mediated inflammation (Li et al, 2015).…”

Section: Mirnas As Potential Therapeutic Targetsmentioning

confidence: 99%

Emerging Roles of miRNAs in Brain Development and Perinatal Brain Injury

et al. 2019

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In human beings the immature brain is highly plastic and depending on the stage of gestation is particularly vulnerable to a range of insults that if sufficiently severe, can result in long-term motor, cognitive and behavioral impairment. With improved neonatal care, the incidence of major motor deficits such as cerebral palsy has declined with prematurity. Unfortunately, however, milder forms of injury characterized by diffuse non-cystic white matter lesions within the periventricular region and surrounding white matter, involving loss of oligodendrocyte progenitors and subsequent axonal hypomyelination as the brain matures have not. Existing therapeutic options for treatment of preterm infants have proved inadequate, partly owing to an incomplete understanding of underlying post-injury cellular and molecular changes that lead to poor neurodevelopmental outcomes. This has reinforced the need to improve our understanding of brain plasticity, explore novel solutions for the development of protective strategies, and identify biomarkers. Compelling evidence exists supporting the involvement of microRNAs (miRNAs), a class of small non-coding RNAs, as important post-transcriptional regulators of gene expression with functions including cell fate specification and plasticity of synaptic connections. Importantly, miRNAs are differentially expressed following brain injury, and can be packaged within exosomes/extracellular vesicles, which play a pivotal role in assuring their intercellular communication and passage across the blood–brain barrier. Indeed, an increasing number of investigations have examined the roles of specific miRNAs following injury and regeneration and it is apparent that this field of research could potentially identify protective therapeutic strategies to ameliorate perinatal brain injury. In this review, we discuss the most recent findings of some important miRNAs in relation to the development of the brain, their dysregulation, functions and regulatory roles following brain injury, and discuss how these can be targeted either as biomarkers of injury or neuroprotective agents.

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Effects of MicroRNA-592-5p on Hippocampal Neuron Injury Following Hypoxic-Ischemic Brain Damage in Neonatal Mice - Involvement of PGD2/DP and PTGDR

Cited by 22 publications

References 45 publications

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

Effects of hydrogen on polarization of macrophages and microglia in a stroke model

Emerging Roles of miRNAs in Brain Development and Perinatal Brain Injury

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