Down-regulated microRNA-183 mediates the Jak/Stat signaling pathway to attenuate hippocampal neuron injury in epilepsy rats by targeting Foxp1

Feng, Xiangyong; Xiong, Wei; Yuan, Mingqiong; Zhan, Jian; Zhu, Xiankun; Wei, Zhijie; Chen, Xidong; Cheng, Xianbing

doi:10.1080/15384101.2019.1671717

Cited by 22 publications

(14 citation statements)

References 31 publications

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“…For instance, down-regulating miR-183 inactivates the Jak/Stat signaling pathway by up-regulating Foxp1, thereby strengthening neuronal proliferation and inhibiting apoptosis of hippocampal neurons in epilepsy rats. 36 Additionally, miR-200a silencing protects neural stem cells from OGD/R-induced damage by regulating the STATs/c-Myc and MAPK/c-Myc signaling pathways. 37 Here, we found that STAT1 and NF-κB were up-regulated in the injured cortex of MCAO mice and BV2 cells induced by OGD/R.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Long Noncoding RNA SNHG15 Ameliorates Hypoxia/Ischemia-Induced Neuronal Damage by Regulating miR-302a-3p/STAT1/NF-κB Axis

et al. 2021

Yonsei Med J

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Purpose Ischemic brain injury results in high mortality and serious neurologic morbidity. Here, we explored the role of SNHG15 in modulating neuronal damage and microglial inflammation after ischemia stroke. Materials and Methods The hypoxia/ischemia models were induced by middle cerebral artery occlusion in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. Quantitative real-time PCR (qRT-PCR) and Western blot were conducted to determine the levels of SNHG15, miR-302a-3p, and STAT1/NF-κB. Moreover, gain- or loss-of functional assays of SNHG15 and miR-302a-3p were conducted. MTT assay was used to evaluate the viability of HT22 cells, and the apoptotic level was determined by flow cytometry. Furthermore, enzyme-linked immunosorbent assay was performed to detect oxidative stress and inflammatory mediators in the ischemia cortex and OGD/R-treated BV2 microglia. Results The SNHG15 and STAT1/NF-κB pathways were both distinctly up-regulated, while miR-302a-3p was notably down-regulated in the ischemia cortex. Additionally, overexpressing SNHG15 dramatically enhanced OGD/R-mediated neuronal apoptosis as well as the expression of oxidative stress and inflammation factors from microglia. In contrast, knocking down SNHG15 or overexpressing miR-302a-3p relieved OGD/R-mediated neuronal apoptosis and microglial activation. Moreover, the rescue experiment testified that overexpressing miR-302a-3p also attenuated SNHG15 up-regulation-induced effects. In terms of the mechanisms, SNHG15 sponged miR-302a-3p and activated STAT1/NF-κB as a competitive endogenous RNA, while miR-302a-3p targeted STAT1 and negatively regulated the STAT1/NF-κB pathway. Conclusion SNHG15 was up-regulated in the hypoxia/ischemia mouse or cell model. The inhibition of SNHG15 ameliorates ischemia/hypoxia-induced neuronal damage and microglial inflammation by regulating the miR-302a-3p/STAT1/NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Long Noncoding RNA SNHG15 Ameliorates Hypoxia/Ischemia-Induced Neuronal Damage by Regulating miR-302a-3p/STAT1/NF-κB Axis

et al. 2021

Yonsei Med J

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“…28 What is more, the level of STAT1 is up-regulated in epilepsy rats' hippocampal tissues. 29 Furthermore, a study observes an increase in STAT1 expression in kidney biopsies with diabetic kidney disease. 30 A new finding of this study was that silenced EZH2 elevated miR-139-5p and decreased STAT1 in HASMCs and arterial tissues of mice.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, EHZ2 has been observed to be up‐regulated obviously after fluoride exposure 28 . What is more, the level of STAT1 is up‐regulated in epilepsy rats' hippocampal tissues 29 . Furthermore, a study observes an increase in STAT1 expression in kidney biopsies with diabetic kidney disease 30 …”

Section: Discussionmentioning

confidence: 99%

Enhancer of zeste homolog 2 participates in the process of atherosclerosis by modulating microRNA‐139‐5p methylation and signal transducer and activator of transcription 1 expression

et al. 2020

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Atherosclerosis (AS) is the main cause of coronary heart disease, in which enhancer of zeste homolog 2 (EZH2) has been implied to participate in this process. Thus, this work proposed to explore the effect of EZH2 on AS from microRNA‐139‐5p (miR‐139‐5p)/signal transducer and activator of transcription 1 (STAT1) axis. EZH2, miR‐139‐5p, and STAT1 expression in arterial tissues of AS patients were detected. Human arterial smooth muscle cells (HASMCs) induced with oxidized low‐density lipoprotein (ox‐LDL) and the mice fed with high fat diet were treated with silenced EZH2 or upregulated miR‐139‐5p to explore their roles in proliferation and apoptosis of HASMCs, together with inflammation response and oxidative stress of mice. Chromatin immunoprecipitation experiment was applied to verify the regulatory effect of EZH2 on miR‐139‐5p through methylation of H3K27me3. The targeting relationship between miR‐139‐5p and STAT1 was verified by online website and luciferase activity assay. Reduced miR‐139‐5p and overexpressed EHZ2 and STAT1 were found in AS. Silenced EZH2 or elevated miR‐139‐5p decreased the production of cholesterol and inhibited inflammation reaction in serum of mice with AS. Silenced EZH2 or elevated miR‐139‐5p facilitated proliferation and restrained apoptosis of ox‐LDL‐treated HASMCs, and restrained oxidative stress and cell apoptosis in arterial tissues of AS mice. EZH2 regulated miR‐139‐5p through H3K27me3, and miR‐139‐5p targeted STAT1. miR‐139‐5p silencing antagonized the effects of EZH2 down‐regulation on AS. This study manifests that down‐regulated EZH2 or elevated miR‐139‐5p inhibits ox‐LDL‐induced HASMCs apoptosis, plaque formation, and inflammatory response in AS mice, which may be related to down‐regulated STAT1.

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“…Here, we focused on the role of signal transducer and activator of transcription 3 (STAT3) in the adult cerebellum. STAT3 is an essential transcription factor for survival, growth, protection, and metabolic regulation (Murase et al, 2012, Bareyre et al, 2011, Feng et al, 2019, Desai and Harris, 2015. At the behavioral level, STAT3 has a direct impact on multiple animal behaviors, such as running, food-intake, and pain (Mesaros et al, 2008, Herrmann et al, 2008, Fernandes et al, 2015, Buettner et al, 2006, Desai and Harris, 2015, Hu et al, 2020, Guo et al, 2018.…”

Section: Introductionmentioning

confidence: 99%

Ablation of STAT3 in Purkinje Cells Reorganizes Cerebellar Synaptic Plasticity in Long-Term Fear Memory Network

Han

Kwon

Kim

et al. 2020

Preprint

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Emotional memory processing, such as fear memory, engages a large neuronal network of brain regions including the cerebellum. However, the molecular and cellular mechanisms of the cerebellar cortex modulating the fear memory network is largely unknown. Here, we illustrate a novel mechanism by which synaptic signaling in cerebellar Purkinje cells (PCs) via STAT3 regulates long-term fear memory. Firstly, we generated PC-specific STAT3 knockout (STAT3PKO) mice. Transcriptome analyses revealed that STAT3 deletion results in transcriptional changes that lead to an increase in the expression of glutamate receptors. The amplitude of AMPA receptor-mediated excitatory postsynaptic currents at parallel fiber to PC synapses was larger in STAT3PKO mice than in wild-type littermates. Conditioning at the parallel fiber induced long-term depression of parallel fiber-PC synapses in STAT3PKO mice while the same manipulation induced long-term potentiation in wild-type littermates. Interestingly, STAT3PKO mice showed an aberrantly enhanced long-term fear memory. Neuronal activity in fear-related regions increased in fear-conditioned STAT3PKO mice. Our data suggest that STAT3-dependent molecular regulation in PCs is indispensable for proper expression of fear memory processing.

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Down-regulated microRNA-183 mediates the Jak/Stat signaling pathway to attenuate hippocampal neuron injury in epilepsy rats by targeting Foxp1

Cited by 22 publications

References 31 publications

Inhibition of Long Noncoding RNA SNHG15 Ameliorates Hypoxia/Ischemia-Induced Neuronal Damage by Regulating miR-302a-3p/STAT1/NF-κB Axis

Inhibition of Long Noncoding RNA SNHG15 Ameliorates Hypoxia/Ischemia-Induced Neuronal Damage by Regulating miR-302a-3p/STAT1/NF-κB Axis

Enhancer of zeste homolog 2 participates in the process of atherosclerosis by modulating microRNA‐139‐5p methylation and signal transducer and activator of transcription 1 expression

Ablation of STAT3 in Purkinje Cells Reorganizes Cerebellar Synaptic Plasticity in Long-Term Fear Memory Network

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