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

Rao, Gaofeng; Zhang, Wenfu; Song, Shegeng

doi:10.3892/mmr.2019.10317

Cited by 9 publications

(8 citation statements)

References 43 publications

(54 reference statements)

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“…They are involved in various cellular physiological processes, such as energy metabolism, oxidative stress, and apoptosis. Their ability to resist oxidative stress has been widely studied in cerebral ischemia-reperfusion (Hou et al, 2010;Rothgiesser et al, 2010;Morris et al, 2011;She et al, 2018;Wang et al, 2018;Wu D. et al, 2018;Chang et al, 2019;Duan et al, 2019;Fusco et al, 2019;Rao et al, 2019;Xian et al, 2019;Zhao B. et al, 2019). SIRT1 activates the FOXO family, and FOXO3a has the ability to resist anti-oxidative stress and enhances ROS scavenging activity (Hou et al, 2010).…”

Section: Sirt/foxo Signaling Pathwaymentioning

confidence: 99%

“…SIRT1 also activates the peroxisome proliferator-activated receptor γ coactivator-1PGC1α (a transcriptional coactivator of oxidative stress) and exerts an antioxidant effect (Morris et al, 2011). By targeting SIRT1 or regulating the SIRT1 related pathway, neurons will be protected from CIRI-induced mitochondrial oxidative stress and inflammatory response (Duan et al, 2019;Fusco et al, 2019;Rao et al, 2019;Xian et al, 2019). Inflammatory cytokines can enhance the activity of SIRT2 in cells, enhance its deacetylation of NF-κB, reduce the transcriptional activity of NF-κB, and reduce the expression of inflammatory mediators, such as interleukin-6 (IL-6), matrix metalloproteinase 9 (MMP9), and cyclooxygenase-2 (COX-2), to exert antioxidant and anti-inflammatory effects (Rothgiesser et al, 2010).…”

Section: Sirt/foxo Signaling Pathwaymentioning

confidence: 99%

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Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

299

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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Section: Sirt/foxo Signaling Pathwaymentioning

confidence: 99%

Section: Sirt/foxo Signaling Pathwaymentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

299

197

View full text Add to dashboard Cite

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“…Although glucose and oxygen deprivation can be attenuated by reperfusion of cerebral blood, the process of reperfusion exacerbates the inflammatory response, oxidative stress and apoptosis, which further aggravates the progression of cerebral damage caused by reperfusion (31)(32)(33). Previous studies have demonstrated that the inhibition of the inflammatory response, oxidative stress and apoptosis rescued cells from OGD/R injury (34,35). Gaire et al (36) reported that Terminalia chebula extract prevented OGD/R injury in PC12 cells and suppressed lipopolysaccharide-induced activation of microglia through inhibition of the oxidative and inflammatory processes.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of the knockdown of lncRNA AK139328 against oxygen glucose deprivation/reoxygenation-induced injury in PC12 cells

2021

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Cerebral ischemic stroke is a major cause of adult morbidity and mortality worldwide. Several long non-coding RNAs (lncRNAs) have been reported to participate in cerebral ischemia/reperfusion injury (IRI). However, to the best of our knowledge, the role of lncRNA AK139328 in cerebral ischemic stroke remains poorly understood. The present study aimed to determine the expression and function of lncRNA AK139328 in the progression of IRI. PC12 cells were injured by oxygen glucose deprivation/reoxygenation (OGD/R) to establish an in vitro ischemic stroke model. An MTT assay was performed to determine cell viability. Reverse transcription-quantitative PCR was used to analyze the expression levels of AK139328 and Netrin-1 in blood samples from patients who had suffered a cerebral ischemic stroke and healthy individuals or OGD/R PC12 cells. ELISAs were used to determine the levels of inflammatory cytokines. In addition, oxidative stress levels and the levels of cell apoptosis were evaluated by reactive oxygen species (ROS) kits, flow cytometry and western blotting. Immunofluorescence staining was used for the detection of cell neurite outgrowth. The results of the present study revealed that AK139328 expression levels were upregulated in patients who had suffered a cerebral ischemic stroke and in PC12 cells following stimulation with OGD/R. The knockdown of AK139328 alleviated OGD/R-induced decreases in cell viability, downregulation in Netrin-1 expression and increases in inflammatory cytokines levels, including TNF-α, IL-1β and IL-6. Moreover, AK139328 silencing suppressed oxidative stress and cell apoptosis in OGD/R-treated PC12 cells. Furthermore, the expression levels of microtubule associated protein 2 and growth associated protein 43 in OGD/R-injured PC12 cells were upregulated following the knockdown of AK139328 expression. In conclusion, these findings suggested that the knockdown of AK139328 expression may protect PC12 cells against OGD/R injury by regulating inflammatory responses, oxidative stress and cell apoptosis. The data suggested a potential therapeutic target for the diagnosis and treatment of cerebral ischemic stroke.

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“…For instance, Yin et al (Yin et al 2010) rst reported that miR-497 aggravated ischemic neuronal death by directly binding to the predicted 3'UTR target sites of Bcl-2/Bcl-w genes. Similarly, downregulation of miR-217 signi cantly ameliorated oxygen-glucose deprivation and reoxygenation (OGD/R)-induced neuron injury, in ammatory responses and oxidative stress by targeting sirtuin 1 (SIRT1) (Rao et al 2019). Inversely, miR-132 could attenuate cerebral injury by protecting blood-brain barrier disruption in ischemia stroke (Zuo et al 2019).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miR-499a-5p Decreases Cerebral Ischemia/Reperfusion Injury by Targeting PDCD4

Shan

Chen

et al. 2021

Cell Mol Neurobiol

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MiR-499a-5p was signi cantly down-regulated in degenerative tissues and correlated with apoptosis.Nonetheless, the biological function of miR-499a-5p in acute ischemic stroke has been still unclear. In this study, we found the plasma levels of miR-499a-5p were signi cantly down-regulated in 64 ischemic stroke patients and negatively correlated with the National Institutes of Health Stroke Scale score. Then, we constructed cerebral ischemia/reperfusion (I/R) injury in rats after middle cerebral artery occlusion and subsequent reperfusion and oxygen-glucose deprivation and reoxygenation (OGD/R) treated SH-SY5Y cell model. Transfection with miR-499a-5p mimic was accomplished by intracerebroventricular injection in the in vivo I/R injury model. We further found miR-499a-5p overexpression decreased infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining. PDCD4 was a direct target of miR-499a-5p by luciferase report assay and western blotting. Knockdown of PDCD4 reduced the infarct damage and cortical neuron apoptosis caused by I/R injury. MiR-499a-5p exerted neuroprotective roles mainly through inhibiting PDCD4-mediated apoptosis by CCK-8 assay, LDH release assay and ow cytometry analysis. These ndings suggest that miR-499a-5p might represent a novel target that regulates brain injury by inhibiting PDCD4-mediating apoptosis.

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

Cited by 9 publications

References 43 publications

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Protective effects of the knockdown of lncRNA AK139328 against oxygen glucose deprivation/reoxygenation-induced injury in PC12 cells

Upregulation of miR-499a-5p Decreases Cerebral Ischemia/Reperfusion Injury by Targeting PDCD4

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