Long non-coding RNA ZFAS1 exerts a protective role to alleviate oxygen and glucose deprivation-mediated injury in ischemic stroke cell model through targeting miR-186-5p/MCL1 axis

2021 ◽  
Author(s):  
Bin Shen ◽  
Lan Wang ◽  
Yuejun Xu ◽  
Hongwei Wang ◽  
Shiyi He
Keyword(s):  
Ischemic Stroke ◽  
Cell Model ◽  
Glucose Deprivation ◽  
Protective Role ◽  
Oxygen And Glucose Deprivation ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA MEG3 alters neuronal apoptosis and is associated with poor prognosis in ischemic stroke: based on basic and prospective studies

2019 ◽  
Author(s):  
Meiping Wang ◽  
Wenjuan Chen ◽  
Yu Geng ◽  
Chenghua Xu ◽  
Xiaoxiao Tao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Poor Prognosis ◽  
Infarct Volume ◽  
High Sensitivity ◽  
Glucose Deprivation ◽  
Expression Level ◽  
Control Group ◽  
Blood Leukocytes ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background: Ischemic stroke (IS) is a highly heterogeneous disease with variable pathogenesis. Due to the lack of early predictive markers, the mortality rate of IS remains high worldwide. This study focused on the expression pattern of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and its prognostic value in IS. Methods: Twenty-four ICR mice (30-35g, 12 males and 12 females) were involved in this study. Middle cerebral artery occlusion (MCAO) was established to simulate an IS environment. Oxygen-glucose deprivation/reoxygenation (OGD/R) in cells were also performed. A total of 215 IS patients and 153 age and gender-matched controls were included. Quantitative Real-time PCR (qRT-PCR) was performed to detect the expression of MEG3 in peripheral blood leukocytes. Results: The MEG3 expression in MCAO group was significantly higher than control group (P=0.004), and the survival time of high MEG3 group was significantly lower than that of the low MEG3 group (P=0.042). OGD/R promotes cell apoptosis, while si-MEG3 inhibits apoptosis. Results of WB showed that, expression level of Bax was down regulated by si-MEG3, while OGD/R increased its expression level. MEG3 was significantly up-regulated in IS patients and associated with the National Institutes of Health Stroke Scale (NIHSS) (r=0.347, P<0.001), modified Rankin Scale (mRS) (r=0.385, P<0.001), high sensitivity C-reactive protein (Hs-CRP) (r=0.221, P=0.002) level and infarct volume (r=0.201, P=0.006). Overall survival analysis showed that patients with higher MEG3 expression had a relatively poor prognosis (P<0.001). Meanwhile, multivariate analysis revealed that MEG3 was an independent prognostic marker of functional outcome and death in patients with IS. Conclusions: Current study suggested that MEG3 might be considered as a potential prognostic indicator in IS.

scholarly journals Up-regulation of miR-499a-5p decreases cerebral ischemia/reperfusion injury by targeting PDCD4

2021 ◽  
Author(s):  
Weifeng Shan ◽  
Huifeng Ge ◽  
Bingquan Chen ◽  
Linger Huang ◽  
Shaojun Zhu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Tunel Staining ◽  
Cerebral Ischemia Reperfusion

Abstract MiR-499a-5p was significantly 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 significantly 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 flow cytometry analysis. These findings suggest that miR-499a-5p might represent a novel target that regulates brain injury by inhibiting PDCD4-mediating apoptosis.

Long non-coding RNA SNHG16, binding with miR-106b-5p, promoted cell apoptosis and inflammation in allergic rhinitis by up-regulating leukemia inhibitory factor to activate the JAK1/STAT3 signaling pathway

2021 ◽  
pp. 096032712110356
Author(s):  
Huajing Li ◽  
Fang Quan ◽  
Pengfei Zhang ◽  
Yuan Shao
Keyword(s):  
Allergic Rhinitis ◽  
Cell Apoptosis ◽  
Leukemia Inhibitory Factor ◽  
Cell Model ◽  
Inhibitory Factor ◽  
Luciferase Reporter ◽  
Stat3 Pathway ◽  
Non Coding Rna ◽  
Apoptosis And Inflammation ◽  
Long Non Coding Rna

Allergic rhinitis (AR) is a type I hypersensitive disease. Long non-coding RNA (lncRNA) SNHG16 acts as an oncogene in a variety of tumors and promotes the occurrence of inflammation in many inflammatory diseases. The study aims to investigate the expression of SNHG16 and its potential biological functions in AR. RT-qPCR results showed that the expression of SNHG16 in AR was up-regulated. The AR cell model was constructed by stimulating primary nasal mucosal epithelial cells from AR patients with IL-13. After knocking down the expression of lncRNA SNHG16, cell apoptosis was detected by flow cytometry, and the expression of inflammatory factors was detected by ELISA. The results showed that SNHG16 promoted cell apoptosis and inflammation. Then, bioinformatics analysis was used to screen miRNAs bound with SNHG16. Luciferase reporter gene assay and RNA pull-down experiment were used to verify the relationship. We found that the expression of miR-106b-5p was down-regulated and leukemia inhibitory factor (LIF) expression was up-regulated in the AR cell model. The expression of phospho-Janus kinase 1 and p-signal transducer and activator of transcription 3 (STAT3) were detected by Western blotting. Silencing the expression of LIF could inhibit the activity of JAK1/STAT3 pathway and further inhibit cell apoptosis and the occurrence of inflammation. Then transfected SNHG16 shRNA alone or together with miR-106b-5p antagomir into the AR cell model, we found that silencing the expression of SNHG16 down-regulated the expression of LIF and inhibited the activity of the JAK1/STAT3 pathway, cell apoptosis, and inflammation. However, miR-106b-5p antagomir weakened its inhibitory effects. The role of SNHG16 in AR was further verified by the ovalbumin-induced AR mouse model in vivo. In conclusion, SNHG16 up-regulates LIF expression by binding with miR-106b-5p, thus promoting the activity of JAK1/STAT3 pathway, and promoting the development of AR. These results provide new targets for the treatment of AR and may help reduce the damage caused by AR.

scholarly journals Protective Role of Kv7 Channels in Oxygen and Glucose Deprivation-Induced Damage in Rat Caudate Brain Slices

2015 ◽  
Vol 35 (10) ◽  
pp. 1593-1600 ◽  
Author(s):  
Vincenzo Barrese ◽  
Maurizio Taglialatela ◽  
Iain A Greenwood ◽  
Colin Davidson
Keyword(s):  
Cell Death ◽  
Brain Slices ◽  
Peak Level ◽  
Glucose Deprivation ◽  
Wistar Rat ◽  
Protective Role ◽  
Triphenyltetrazolium Chloride ◽  
Lactate Dehydrogenase Activity ◽  
Oxygen And Glucose Deprivation ◽  
Dopamine Efflux

Ischemic stroke can cause striatal dopamine efflux that contributes to cell death. Since Kv7 potassium channels regulate dopamine release, we investigated the effects of their pharmacological modulation on dopamine efflux, measured by fast cyclic voltammetry (FCV), and neurotoxicity, in Wistar rat caudate brain slices undergoing oxygen and glucose deprivation (OGD). The Kv7 activators retigabine and ICA27243 delayed the onset, and decreased the peak level of dopamine efflux induced by OGD; and also decreased OGD-induced damage measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Retigabine also reduced OGD-induced necrotic cell death evaluated by lactate dehydrogenase activity assay. The Kv7 blocker linopirdine increased OGD-evoked dopamine efflux and OGD-induced damage, and attenuated the effects of retigabine. Quantitative-PCR experiments showed that OGD caused an ~ 6-fold decrease in Kv7.2 transcript, while levels of mRNAs encoding for other Kv7 subunits were unaffected; western blot experiments showed a parallel reduction in Kv7.2 protein levels. Retigabine also decreased the peak level of dopamine efflux induced by L-glutamate, and attenuated the loss of TTC staining induced by the excitotoxin. These results suggest a role for Kv7.2 in modulating ischemia-evoked caudate damage.

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