MicroRNA‐135a alleviates oxygen‐glucose deprivation and reoxygenation‐induced injury in neurons through regulation of GSK‐3β/Nrf2 signaling

Liu, Xiaobin; Li, Min; Hou, Mingshan; Huang, Weidong; Song, Jin‐Ning

doi:10.1002/jbt.22159

Cited by 14 publications

(12 citation statements)

References 54 publications

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“…Primary neuron culture. Primary rat cerebral cortical neurons were extracted from Sprague-dawley rat embryos (n=5) at embryonic day 16-18 as previously described (25,26). in brief, brain cortex tissues were extracted and dissected in Hanks' balanced salt solution (HBSS), cut into ~1 mm 3 cubes, washed with HBSS, and then digested with 0.25% trypsin (37˚C for 15 min).…”

Section: Methodsmentioning

confidence: 99%

“…The oGd/r model was established in the present study as previously described (26). in brief, cortical neurons were plated into 6-well plates at a density of 5x10 5 cells/ml (2 ml) and cultured overnight.…”

Section: Ogd/r Model Establishmentmentioning

confidence: 99%

“…assay. cell viability was determined at 24 h following oGd/r induction as previously described (26). cell viability was determined via a ccK-8 assay.…”

Section: Ogd/r Model Establishmentmentioning

confidence: 99%

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MicroRNA‑217 inhibition relieves cerebral ischemia/reperfusion injury by targeting SIRT1

2019

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Micrornas (mirs) have been proposed to be involved in the pathological processes of cerebral ischemia/reperfusion (cir) injury. The present study aimed to investigate the potential role and molecular mechanisms of mir-217 in the regulation of neuronal survival in cir injury. To perform the investigation, an in vitro cellular model of cir injury was established by treating neurons with oxygen-glucose deprivation and reoxygenation (oGd/r). mir-217 levels in neurons were detected using reverse transcription-quantitative Pcr. The association between miR-217 and sirtuin 1 (SIRT1) was identified using TargetScan and validated in a dual-luciferase reporter assay. cell viability and apoptosis were measured using a cell counting Kit-8 assay and flow cytometry, respectively. The release of lactate dehydrogenase, and the production of proinflammatory factors and oxidative stress biomarkers were analyzed by eliSas and using specific assay kits. It was revealed that miR-217 was significantly upregulated in oGd/r-treated neurons. SirT1 was a direct target of mir-217, and was downregulated in neurons following OGD/R treatment. Downregulation of miR-217 significantly ameliorated oGd/r-induced neuronal injury, inflammatory responses and oxidative stress. The effects of mir-217 inhibitor on oGd/r treated neurons were attenuated by SirT1 knockdown. additionally, western blotting revealed that the SirT1/aMP-activated protein kinase-α/nF-κB pathway was partially involved in the regulation of oGd/r-induced neuronal injury by mir-217. in conclusion, the data of the present study indicated that the downregulation of mir-217 protected neurons against oGd/r-induced injury by targeting SirT1.

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Section: Methodsmentioning

confidence: 99%

Section: Ogd/r Model Establishmentmentioning

confidence: 99%

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MicroRNA‑217 inhibition relieves cerebral ischemia/reperfusion injury by targeting SIRT1

2019

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“…A-kinase anchor protein 7 (AKAP7) is mainly expressed in lymphocytes, which is closely related to the integrity of the blood-brain barrier [45]. In the study of the effect of circRNA on post-stroke transcription [36] factors, finding it expresses increased significantly in peripheral blood after stroke. The circ-015350 generated by the NcoA2 gene is associated with various biological processes such as post-stroke apoptosis and oxidative stress.…”

Section: Circrna Regulates the Progression Of Cerebrovascular Diseasementioning

confidence: 99%

“…In the study of the cerebral ischemia-reperfusion model, Liu et al [36] established a model of glucose oxygen deprivation/reoxygenation in mouse hippocampal neurons HT22 cells, and screened by circRNA microarray, and found that three expressions of circRNA and 12 expressions were decreased. The circRNA, a target circRNAs capable of adsorbing miRNAs through sponges, affects apoptosis and immune-related processes, suggesting involvement in the pathophysiological process of cerebral ischemia-reperfusion injury.…”

Section: Circrna Regulates the Progression Of Cerebrovascular Diseasementioning

confidence: 99%

circRNAs: Potential Targets for the Prevention and Treatment of Cerebrovascular Diseases

Xie

Zhang

et al. 2019

SN Compr. Clin. Med.

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circRNAs, as a kind of non-coding RNA, are characterized by rich content, high stability, and tissue specificity, and have become a research focus in recent years. A large number of studies have found that circRNA and miRNA have the strongest binding capacity among competing endogenous RNAs, playing a role as a miRNA molecular sponge in cellular gene expression and playing an important role in many diseases. At present, studies have shown that circRNAs are closely related to cerebrovascular diseases and play a crucial role in vascular endothelial cells, metabolism of low-density lipoprotein, smooth muscle cells, inflammatory oxidative stress, ischemia-reperfusion, and other regulatory mechanisms. In order to systematically understand circRNA and its function, in order to understand the research progress of circRNA in regulating the molecular mechanism of cerebrovascular diseases, and in order to find potential markers and drug molecules in the field of cerebrovascular disease occurrence, development, diagnosis, and treatment targets, we reviewed the research progress of circRNA in the development of cerebrovascular disease.

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Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

Zhang

Gong

et al. 2019

Journal Cellular Physiology

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Myocardial ischemia/reperfusion injury (MIRI) is a clinically familiar disease, which possesses a great negative impact on human health. But, the effective treatment is still absent. MicroRNAs (miRNAs) have been testified to play a momentous role in MIRI. The purpose of the study aimed to probe the functions of miR-132 in oxygen and glucose deprivation (OGD)-evoked injury in H9c2 cells. miR-132 expression in H9c2 cells accompanied by OGD disposition was evaluated via real-time quantitative polymerase chain reaction. After miR-132 mimic and inhibitor transfections, the impacts of miR-132 on OGD-affected H9c2 cell viability, apoptosis, cell cycle, and the interrelated factors were appraised by exploiting cell counting kit-8, flow cytometry, and western blot analysis. FOXO3A expression was estimated in above-transfected cells, meanwhile, the correlation between miR-132 and FOXO3A was probed by dualluciferase report assay. Ultimately, above mentioned cell processes were reassessed in H9c2 cells after preprocessing OGD administration and transfection with si-FOXO3A and si-NC plasmids. We got that OGD disposition obviously enhanced miR-132 expression in H9c2 cells. Overexpressed miR-132 evidently reversed OGDevoked cell viability repression and apoptosis induction in H9c2 cells. In addition, overexpressed miR-132 mitigated OGD-evoked G0/G1 cell arrest by mediating p21, p27, and cyclin D1 expression. Repression of FOXO3A was observed in miR-132mimic-transfected cells, which was also predicated as a direct gene of miR-132. We discovered that silenced FOXO3A alleviated OGD-evoked cell injury in H9c2 cells via facilitating cell viability, hindering apoptosis and restraining cell arrest at G0/G1 phase. In conclusion, these investigations corroborated that miR-132 exhibited the protective impacts on H9c2 cells against OGD-evoked injury via targeting FOXO3A.

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MicroRNA‐135a alleviates oxygen‐glucose deprivation and reoxygenation‐induced injury in neurons through regulation of GSK‐3β/Nrf2 signaling

Cited by 14 publications

References 54 publications

MicroRNA‑217 inhibition relieves cerebral ischemia/reperfusion injury by targeting SIRT1

MicroRNA‑217 inhibition relieves cerebral ischemia/reperfusion injury by targeting SIRT1

circRNAs: Potential Targets for the Prevention and Treatment of Cerebrovascular Diseases

Retracted: MicroRNA‐132 protects H9c2 cells against oxygen and glucose deprivation‐evoked injury by targeting FOXO3A

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