Circular RNA circPTK2 regulates oxygen-glucose deprivation-activated microglia-induced hippocampal neuronal apoptosis via miR-29b-SOCS-1-JAK2/STAT3-IL-1β signaling

Wang, Huilin; Li, Zheng; Gao, Jingyan; Liao, Qingwu

doi:10.1016/j.ijbiomac.2019.02.041

Cited by 47 publications

(43 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…found that circPTK2 exert critical roles in colorectal cancer (CRC) growth and metastasis, it may serve as a potential therapeutic target for CRC metastasis. The same study also revealed that circPTK2 regulates OGDactivated microglia-induced neuronal apoptosis via miR-29b-SOCS-1-JAK2/STAT3-IL-1βsignaling (Wang H. et al, 2019). In lung cancer, a group of circRNAs have also been found to be significantly dysregulated and several NSCLC-related circRNAs are identified.…”

Section: Introductionmentioning

confidence: 79%

Differential Expression and Bioinformatics Analysis of circRNA in Non-small Cell Lung Cancer

Sun

et al. 2020

Front. Genet.

View full text Add to dashboard Cite

Circular RNA (CircRNA) plays an important role in tumorigenesis and progression of non-small cell lung cancer (NSCLC), but the pathogenesis of NSCLC caused by circRNA has not been fully elucidated. This study aimed to investigate differentially expressed circRNAs and identify the underlying pathogenesis hub genes of NSCLC by comprehensive bioinformatics analysis. Data of gene expression microarrays (GSE101586, GSE101684, and GSE112214) were downloaded from Gene Expression Omnibus (GEO) database. Differentially expressed circRNAs (DECs) were obtained by the “limma” package of R programs and the overlapping operation was implemented of DECs. CircBase database and Cancer-Specific CircRNA database (CSCD) were used to find miRNAs binding to DECs. Target genes of the found miRNAs were identified utilizing Perl programs based on miRDB, miRTarBase, and TargetScan databases. Functional and enrichment analyses of selected target genes were performing using the “cluster profiler” package. Protein-protein interaction (PPI) network was constructed by the Search Tool for the STRING database and module analysis of selected hub genes was performed by Cytoscape 3.7.1. Survival analysis of hub genes were performed by Gene Expression Profiling Interactive Analysis (GEPIA). Respectively, 1 DEC, 249 DECs, and 101 DECs were identified in GSE101586, GSE101684, and GSE112214. A total of eight overlapped circRNAs, 43 miRNAs and 427 target genes were identified. Gene Ontology (GO) enrichment analysis showed these target genes were enriched in biological processes of regulation of histone methylation, Ras protein signal transduction and covalent chromatin modification etc. Pathway enrichment analysis showed these target genes are mainly involved in AMPK signaling pathway, signaling pathways regulating pluripotency of stem cells and insulin signaling pathway etc. A PPI network was constructed based on 427 target genes of the 43 miRNAs. Ten hub genes were found, of which the expression of MYLIP, GAN, and CDC27 were significantly related to NSCLC patient prognosis. Our study provide a deeper understanding the circRNAs-miRNAs-target genes by bioinformatics analysis, which may provide novel insights for unraveling pathogenesis of NSCLC. MYLIP, GAN, and CDC27 genes might serve as novel biomarker for precise treatment and prognosis of NSCLC in the future.

show abstract

Section: Introductionmentioning

confidence: 79%

Differential Expression and Bioinformatics Analysis of circRNA in Non-small Cell Lung Cancer

Sun

et al. 2020

Front. Genet.

View full text Add to dashboard Cite

show abstract

“…Previous studies have shown that the upregulation of miR-29b in microglia inhibits the JAK-2/STAT3 signaling pathway by promoting the expression of SOCS-1; thus suppressing the production of IL-1β. Furthermore, miR-29b inhibition can regulate microglial-induced apoptosis of hippocampal neurons via the JAK-2/STAT3 pathway (Wang et al, 2019a). In an oxygen-glucose deprivation/reperfusion injury model or MCAO model, miR-145-5p was significantly upregulated in microglia.…”

Section: Mirnas Regulate Inflammation Via Other Pathwaysmentioning

confidence: 95%

“…Certain miRNAs, such as miR-26a (Kumar et al, 2015), miR-377 (Fan et al, 2018), miR-200b (Jadhav et al, 2014), miR-3473b (Wang et al, 2018b), miR-101a (Saika et al, 2017), let-7c-5p (Ni et al, 2015), miR-29b (Wang et al, 2019a), and miR-145-5p (Xie et al, 2017) were differentially expressed following ischemia and were shown to work through specific proteins and signaling pathways. Downregulation of miR-26a increased the expression of activating transcription factor 2 (ATF2), which led to increased production of IL-6.…”

Section: Mirnas Regulate Inflammation Via Other Pathwaysmentioning

confidence: 99%

Neuroinflammation in Ischemic Stroke: Focus on MicroRNA-mediated Polarization of Microglia

Lian

Yun-sha

Liu

et al. 2021

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Ischemic stroke is one of the most common causes of death and disability worldwide. Neuroinflammation is a major pathological event involved in the process of ischemic injury and repair. In particular, microglia play a dual role in neuroinflammation. During the acute phase of stroke onset, M2 microglia are the dominant phenotype and exert protective effects on neuronal cells, whereas permanent M1 microglia contribute to prolonged inflammation and are detrimental to brain tissue. Emerging evidence indicates that microRNAs (miRNAs) may have regulatory effects on microglia-associated inflammation. Thus, we briefly reviewed the dynamic response of microglia after a stroke and assessed how specific miRNAs affect the behavior of reactive microglia. We concluded that miRNAs may be useful novel therapeutic targets to improve stroke outcomes and modulate neuroinflammation.

show abstract

“…An investigation on the PD model showed that upregulated miR-155 overexpresses SOCS1 gene expression, which triggers JAK/STAT pathway [ 46 ]. Another study performed by Wang et al, 2018 demonstrated that circPTK2 sponges with miR-29b and activate SOCS-1-JAK2/STAT3-IL-1β signal transduction which causes microglia activation and inflammatory factor secretion, leading to neuronal apoptosis [ 201 ]. In another study, downregulation of DNMT1 in nestatin-positive NPCs enhanced GFAP and S100 expression and resulted in JAK/STAT pathway, including STAT1 and STAT3 [ 202 ].…”

Section: Synergistic Epigenetic Regulation and Pdmentioning

confidence: 99%

Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease

Rasheed

Liang

Wang

et al. 2021

IJMS

View full text Add to dashboard Cite

Neuroinflammation is one of the most significant factors involved in the initiation and progression of Parkinson’s disease. PD is a neurodegenerative disorder with a motor disability linked with various complex and diversified risk factors. These factors trigger myriads of cellular and molecular processes, such as misfolding defective proteins, oxidative stress, mitochondrial dysfunction, and neurotoxic substances that induce selective neurodegeneration of dopamine neurons. This neuronal damage activates the neuronal immune system, including glial cells and inflammatory cytokines, to trigger neuroinflammation. The transition of acute to chronic neuroinflammation enhances the susceptibility of inflammation-induced dopaminergic neuron damage, forming a vicious cycle and prompting an individual to PD development. Epigenetic mechanisms recently have been at the forefront of the regulation of neuroinflammatory factors in PD, proposing a new dawn for breaking this vicious cycle. This review examined the core epigenetic mechanisms involved in the activation and phenotypic transformation of glial cells mediated neuroinflammation in PD. We found that epigenetic mechanisms do not work independently, despite being coordinated with each other to activate neuroinflammatory pathways. In this regard, we attempted to find the synergic correlation and contribution of these epigenetic modifications with various neuroinflammatory pathways to broaden the canvas of underlying pathological mechanisms involved in PD development. Moreover, this study highlighted the dual characteristics (neuroprotective/neurotoxic) of these epigenetic marks, which may counteract PD pathogenesis and make them potential candidates for devising future PD diagnosis and treatment.

show abstract

Circular RNA circPTK2 regulates oxygen-glucose deprivation-activated microglia-induced hippocampal neuronal apoptosis via miR-29b-SOCS-1-JAK2/STAT3-IL-1β signaling

Cited by 47 publications

References 41 publications

Differential Expression and Bioinformatics Analysis of circRNA in Non-small Cell Lung Cancer

Differential Expression and Bioinformatics Analysis of circRNA in Non-small Cell Lung Cancer

Neuroinflammation in Ischemic Stroke: Focus on MicroRNA-mediated Polarization of Microglia

Epigenetic Regulation of Neuroinflammation in Parkinson’s Disease

Contact Info

Product

Resources

About