Journal of Molecular Neuroscience最新文献

{"title":"Decoding the Role of Kinesin Superfamily Proteins in Glioma Progression.","authors":"Mohamed J Saadh, Zahraa Sabah Ghnim, Morug Salih Mahdi, Muktesh Chandra, Suhas Ballal, Lakshay Bareja, Kamlesh Chaudhary, R S K Sharma, Sofia Gupta, Waam Mohammed Taher, Mariem Alwan, Mahmood Jasem Jawad, Atheer Khdyair Hamad","doi":"10.1007/s12031-025-02308-9","DOIUrl":"https://doi.org/10.1007/s12031-025-02308-9","url":null,"abstract":"<p><p>Glioma is a highly aggressive and invasive brain tumor with limited treatment options, highlighting the need for novel therapeutic approaches. Kinesin superfamily proteins (KIFs) are a diverse group of motor proteins that play essential roles in cellular processes such as mitosis, intracellular transport, and signal transduction, all of which are crucial for tumorigenesis. This review focuses on the multifaceted role of KIFs in glioma, examining their clinical relevance, contribution to tumor progression, and potential as therapeutic targets. We discuss how KIFs influence key aspects of glioma biology, including cell proliferation, invasion, migration, and metastasis. Furthermore, we explore the regulation of the cell cycle and critical signaling pathways associated with glioma, such as PI3K-Akt, Wnt/β-catenin, and Hedgehog signaling by KIFs. The review also addresses the emerging interplay between KIFs and non-coding RNAs, including circular RNAs (circRNAs) and microRNAs (miRNAs), in glioma progression. Finally, we examine current therapeutic strategies targeting KIFs, including immunotherapy, chemotherapy, and small-molecule inhibitors, and their potential to improve treatment outcomes for glioma patients. By synthesizing these insights, this review underscores the significance of KIFs in glioma pathogenesis and their promise as novel therapeutic targets in the fight against glioma.</p>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":"10"},"PeriodicalIF":2.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143021487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of the Dysregulation of circRNAs Expression in Glioblastoma Multiforme","authors":"Yafei Wang,&nbsp;Ying Yu,&nbsp;Jiahua Yu,&nbsp;Cheng Wang,&nbsp;Yunkun Wang,&nbsp;Runxi Fu,&nbsp;Chenran Zhang","doi":"10.1007/s12031-024-02285-5","DOIUrl":"10.1007/s12031-024-02285-5","url":null,"abstract":"<div><p>Primary brain tumors that were the most severe and aggressive were called glioblastoma multiforme (GBM). Cancers are caused in part by aberrant expression of circular RNA. Often referred to as competitive endogenous RNA (ceRNA), circRNA molecules act as “miRNA sponges” in cells by decreasing the inhibitory impact of miRNA on their target genes and hence raising the expression levels of those genes. circRNA molecules are rich in miRNA binding sites. The discovery of more structurally diverse and GBM-related circRNAs has great promise for the use of GMB prognostic biomarkers and therapeutic targets, as well as for comprehending the molecular regulatory mechanisms of GBM. In this work, we present an overview of the circRNA expression patterns associated with GBM and offer a potential integrated electrochemical strategy for detecting circRNA with extreme sensitivity in the diagnosis of glioblastoma.</p><h3>Graphical Abstract</h3><p>The circular RNA (circRNA) regulates both physiological and pathological processes in glioblastoma multiforme disease. Hence, it could serve as a biomarker as well as a therapeutic target.</p>\u0000<div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142995624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic Value of Serum miR-499a-5p in Chinese Children with Autism Spectrum Disorders","authors":"Jie Ren,&nbsp;Yanle Bai,&nbsp;Jielin Gao,&nbsp;Yafei Hou,&nbsp;Jie Mao,&nbsp;Fengxiao Gao,&nbsp;Jiaqi Wang","doi":"10.1007/s12031-024-02296-2","DOIUrl":"10.1007/s12031-024-02296-2","url":null,"abstract":"<div><p>The purpose of this study was to investigate the expression of miR-499a-5p in children with autism spectrum disorders (ASD) and its value in early diagnosis of ASD. This is a retrospective case–control study that included 40 children with ASD as a case group and 43 healthy children as a control group. Magnetic resonance imaging (MRI) was performed on all subjects, and the children were scored with childhood autism rating scale (CARS) and autism behavior checklist (ABC). The expression of miR-499a-5p in serum was detected by RT-qPCR, and the diagnostic value of miR-499a-5p in ASD was evaluated by ROC curve. Pearson correlation coefficient was used to evaluate the correlation between miR-499a-5p levels and scores. Compared with healthy children, the expression level of serum miR-499a-5p was significantly reduced in children with ASD. ROC curve showed that miR-499a-5p is of high diagnostic value for ASD. The results of MRI suggested that the volume of the amygdala in ASD children was significantly larger than that in healthy children, while the volume of the caudate nucleus was significantly reduced. Correlation results showed that the scores of CARS and ABC in the ASD group were significantly negatively correlated with the levels of miR-499a-5p. In the ASD group, the volume of the amygdala was negatively correlated with the level of miR-499a-5p, while the volume of the caudate nucleus was positively correlated with the level of miR-499a-5p. The decreased expression of miR-499a-5p in the serum of children with ASD was significantly related to the changes in brain volume of children with ASD, and the miRNA showed good diagnostic accuracy in children with ASD.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142995755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Brain Imaging and Genetic Risk Factors in Different Progression States of Alzheimer’s Disease Through OSnetNMF-Based Methods","authors":"Min Gao,&nbsp;Wei Kong,&nbsp;Kun Liu,&nbsp;Gen Wen,&nbsp;Yaling Yu,&nbsp;Yuemin Zhu,&nbsp;Zhihan Jiang,&nbsp;Kai Wei","doi":"10.1007/s12031-024-02274-8","DOIUrl":"10.1007/s12031-024-02274-8","url":null,"abstract":"<div><p>Alzheimer's disease (AD) is a neurodegenerative disease with no effective treatment, often preceded by mild cognitive impairment (MCI). Multimodal imaging genetics integrates imaging and genetic data to gain a deeper understanding of disease progression and individual variations. This study focuses on exploring the mechanisms that drive the transition from normal cognition to MCI and ultimately to AD. As an effective joint feature extraction and dimensionality reduction method, non-negative matrix factorization (NMF) and its improved variants, particularly the network-based non-negative matrix factorization (netNMF), have been widely used in multimodal analysis to mine brain imaging and genetic data by considering the interactions between different features. However, many of these methods overlook the importance of the coefficient matrix and do not address issues related to data accuracy and feature redundancy. To address these limitations, we propose an orthogonal sparse network non-negative matrix factorization (OSnetNMF) algorithm, which introduces orthogonal and sparse constraints based on netNMF. By establishing linear relationships between structural magnetic resonance imaging (sMRI) and corresponding gene expression data, OSnetNMF reduces feature redundancy and decreases correlation between data, resulting in more accurate and reliable biomarker extraction. Experiments demonstrate that the OSnetNMF algorithm can accurately identify risk regions of interest (ROIs) and key genes that characterize AD progression, revealing significant trends in ROI pairs such as l4thVen-HIF1A, rBst-MPO, and rBst-PTK2B. Comparative experiments show that the improved algorithm outperforms traditional methods, identifying more disease-related biomarkers and achieving better reconstruction performance.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142994546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision Prediction of Alzheimer’s Disease: Integrating Mitochondrial Energy Metabolism and Immunological Insights","authors":"Wenlong Du,&nbsp;Shihui Yu,&nbsp;Ruiyao Liu,&nbsp;Qingqing Kong,&nbsp;Xin Hao,&nbsp;Yi Liu","doi":"10.1007/s12031-024-02291-7","DOIUrl":"10.1007/s12031-024-02291-7","url":null,"abstract":"<div><p>Alzheimer’s disease (AD), a prevalent neurodegenerative disorder, is characterized by mitochondrial dysfunction and immune dysregulation. This study is aimed at developing a risk prediction model for AD by integrating multi-omics data and exploring the interplay between mitochondrial energy metabolism-related genes (MEMRGs) and immune cell dynamics. We integrated four GEO datasets (GSE132903, GSE29378, GSE33000, GSE5281) for differential gene expression analysis, functional enrichment, and weighted gene co-expression network analysis (WGCNA). We identified two key gene modules (turquoise and magenta) significantly correlated with AD. Subsequently, we constructed a risk prediction model incorporating five MEMRGs (MRPL15, RBP4, ABCA1, MPV17, and MRPL37) and clinical factors using LASSO regression. The model demonstrated robust predictive performance (AUC &gt; 0.815) in both internal and external validation (GSE44770) cohorts. Downregulation of MRPL15, RBP4, MPV17, and MRPL37 in AD brain regions (validated using AlzData and qRT-PCR) suggests impaired mitochondrial function. Conversely, ABCA1 upregulation may represent a compensatory response. Furthermore, significant differences in immune cell proportions, particularly gamma delta T cells (<i>p</i> = 0.002) and activated CD4 memory T cells (<i>p</i> = 0.027), were found between AD and non-demented samples. We observed significant correlations between MEMRG expression and specific immune cell fractions, indicating a potential link between mitochondrial dysfunction and immune dysregulation in AD. Our study provides a reliable risk prediction model for AD and highlights the crucial roles of MEMRGs and immune responses in disease pathogenesis, offering potential targets for therapeutic interventions.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Key Biomarkers Associated with Glioma Hemorrhage: Evidence from Bioinformatic Analysis and Clinical Validation","authors":"Zhe Shen,&nbsp;Tao Li,&nbsp;Bo Yang","doi":"10.1007/s12031-024-02294-4","DOIUrl":"10.1007/s12031-024-02294-4","url":null,"abstract":"<div><p>Hemorrhagic stroke is a known complication of glioma, yet the underlying mechanisms remain poorly understood. This study aims to investigate key biomarkers of glioma-related hemorrhage to provide insights into glioma molecular therapies. Data were obtained from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) databases to analyze differentially expressed genes (DEGs) in glioma by contrasting glioblastoma (GBM) with low-grade gliomas (LGGs). We conducted enrichment analyses using the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) databases through the Database for Annotation, Visualization, and Integrated Discovery (DAVID). A STRING-based protein–protein interaction (PPI) network was developed to identify hub genes, which were subsequently analyzed for their functions in the GeneCards database. To identify angiogenesis-associated genes, we utilized the Human Protein Atlas (HPA) and Gene Expression Profiling Interactive Analysis (GEPIA) databases. A clinical pathological study was conducted using immunohistochemistry (IHC) staining to confirm the findings. In the GEO database, the GEO Series Experiments GSE26576 and GSE184941 included 4523 and 1471 differentially expressed genes (DEGs), respectively. We identified 2715 DEGs using the cBioPortal within the TCGA database. A Venn diagram identified 39 common DEGs. The KEGG pathways and Gene Ontology (GO) analysis highlighted functions related to angiogenesis. PPI network analyses pinpointed 13 hub genes. Through cross-referencing a gene set related to tumor angiogenesis in the GeneCards database, we identified MMP-2 and EGFR as key genes. In the HPA database, we observed EGFR and MMP-2 expression in the normal cerebral cortex, confirmed by IHC. In GEPIA database, high MMP-2 levels were associated with decreased survival time, while EGFR expression showed no significant differences in survival. A clinical study of 21 patients, 11 in the control group and 10 in the stroke group with glioma hemorrhage, revealed no significant differences in their characteristics or comorbidities. IDH1 positivity was higher in the control group (4/11) vs the stroke group (0/10). Tumor cells exhibited increased MMP-2 and EGFR expression, with stronger staining in the stroke group. Our study concluded that IDH1, MMP-2, and EGFR are implicated in the molecular mechanism of glioma hemorrhage as key biomarkers. MMP-2 and IDH1 are potential targets for molecular therapy.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142976573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering Necroptosis-Associated Molecular Subtypes in Acute Ischemic Stroke Through Bioinformatics and Machine Learning Analysis","authors":"Zongkai Wu,&nbsp;Hongzhen Fan,&nbsp;Lu Qin,&nbsp;Xiaoli Niu,&nbsp;Bao Chu,&nbsp;Kaihua Zhang,&nbsp;Yaran Gao,&nbsp;Hebo Wang","doi":"10.1007/s12031-024-02241-3","DOIUrl":"10.1007/s12031-024-02241-3","url":null,"abstract":"<div><p>Acute ischemic stroke (AIS) is a severe disorder characterized by complex pathophysiological processes, which can lead to disability and death. This study aimed to determine necroptosis-associated genes in acute ischemic stroke (AIS) and to investigate their potential as diagnostic and therapeutic targets for AIS. Expression profiling data were acquired from the Gene Expression Omnibus database, and necroptosis-associated genes were retrieved from GeneCards. The differentially expressed genes (DEGs) and necroptosis-related genes were intersected to obtain the necroptosis-related DEGs (NRDEGs) in AIS. In AIS, a total of 76 genes associated with necroptosis (referred to as NRDEGs) were identified. Enrichment analysis of these genes revealed that they were primarily enriched in pathways known to induce necroptosis. Using weighted gene co-expression network analysis (WGCNA), five co-expression modules consisting of NRDEGs were identified, along with two modules that exhibited a strong correlation with AIS. Protein–protein interaction (PPI) analysis resulted in the identification of 20 hub genes. The Least absolute shrinkage and selection operator (LASSO) regression model demonstrated promising potential for diagnostic prediction. The receiver operating characteristic (ROC) curve validated the diagnostic model and selected nine characteristic genes that exhibited statistically significant differences (<i>p</i> &lt; 0.05). By employing consensus clustering, distinct patterns of necroptosis were identified using these nine signature genes. The results were validated by quantitative PCR (qPCR) in venous blood from patients with AIS and healthy controls and HT22 cells, as well as external datasets. Furthermore, the analyzed ceRNA network included nine lncRNAs, six miRNAs, and three mRNAs. Overall, this study offers novel insights into the molecular mechanisms underlying NRDEGs in AIS. The findings provide valuable evidence and contribute to our understanding of the disease.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12031-024-02241-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142912996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Don’t Devoid Emotions from Science","authors":"Noam Shomron","doi":"10.1007/s12031-024-02284-6","DOIUrl":"10.1007/s12031-024-02284-6","url":null,"abstract":"","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying the Pathogenicity of a Novel NPRL3 Missense Mutation Using Personalized Cortical Organoid Model of Focal Cortical Dysplasia","authors":"Rongrong Lu,&nbsp;Ying Xu,&nbsp;Hao Li,&nbsp;Man Xiong,&nbsp;Wenhao Zhou,&nbsp;Weijun Feng,&nbsp;Rui Zhao","doi":"10.1007/s12031-024-02304-5","DOIUrl":"10.1007/s12031-024-02304-5","url":null,"abstract":"<div><p>Focal cortical dysplasia (FCD) II is a cortical malformation characterized by cortical architectural abnormalities, dysmorphic neurons, with or without balloon cells. Here, we systematically explored the pathophysiological role of the GATOR1 subunit NPRL3 variants including a novel mutation from iPSCs derived from one FCD II patient. Three FCD II children aged 0.5–7 years who underwent cerebral lesion resection in our hospital from March 2019 to October 2019 were included in this study. We generated patient-derived iPSCs and performed whole-exome sequencing to accurately identify somatic cells with mutations. The effect of the newly identified <i>NPRL3</i> mutation found in one of our FCD II patients was evaluated using the personalized cortical organoid model and the <i>NPRL3</i> knockout HEK293T cells. Whole-exome sequencing of iPSCs derived from FCD II patients revealed a novel NPRL3 C.767G &gt; C (p.R256P) heterozygous mutation. Cortical organoids generated from iPSCs of FCD II patients were larger than control iPSCs, with increased number of p-S6⁺ cells and NeuN⁺ neurons. In <i>NPRL3</i> knockout HEK293T cells, overexpression of NPRL3  together with NPRL2 protein is necessary to reduce p-S6 level upon amino acid starvation. The reduced binding between NPRL3 ^Arg256Pro and NPRL2 protein leads to downregulation of the relative total protein amount of both proteins in the cell. Our study describes a novel cortical organoid model generated from iPSCs of the FCD patients to investigate the underlying mechanism of NPRL3-related epilepsy. The mutation of NPRL3 ^Arg256Pro impaired the function of NPRL3 protein via affecting the binding with NPRL2 protein, which resulted in unstable protein monomer.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142889564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen–Glucose Deprivation/Reoxygenation","authors":"Mohammad Yusuf Hasan,&nbsp;Azim Haikal Md Roslan,&nbsp;Norazrina Azmi,&nbsp;Norlinah Mohamed Ibrahim,&nbsp;Alina Arulsamy,&nbsp;Vanessa Lin Lin Lee,&nbsp;Rosfaiizah Siran,&nbsp;Sharmili Vidyadaran,&nbsp;Eng Wee Chua,&nbsp;Mohd Kaisan Mahadi","doi":"10.1007/s12031-024-02300-9","DOIUrl":"10.1007/s12031-024-02300-9","url":null,"abstract":"<div><p>Elevated inflammatory reactions are a significant component in cerebral ischemia–reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen–glucose deprivation/reoxygenation (OGDR) condition. OGDR significantly increased the gene expression of pro-inflammatory markers such as TNF-α, IL-6, and IL1β, while α7nAChR agonists reduced these markers. The anti-inflammatory gene marker IL-10 was upregulated by α7nAChR agonist treatment. Downstream pathway marker analysis showed that both gene and protein expression of NFκB was associated with anti-inflammatory effects. Blocking microRNA-21 with antagomir reversed the anti-inflammatory effects. NanoString analysis revealed that microRNA-21 inhibition significantly affected inflammation-related genes, including <i>AL1RAP</i>, <i>TLR9</i>, <i>FLT1</i>, <i>PTGIR</i>, <i>NFκB</i>, <i>TREM2</i>, <i>TNF</i>, <i>SMAD7</i>, <i>FOS</i>, <i>CCL5</i>, <i>IFIT1</i>, <i>CFB</i>, <i>CXCL10</i>, <i>IFI44</i>, <i>DDIT3</i>, <i>IRF7</i>, <i>OASL1</i>, <i>IL1A</i>, <i>IFIT2</i>, <i>C3</i>, <i>CD40</i>, <i>STAT2</i>, <i>IFIT3</i>, <i>IL1RN</i>, <i>OAS1A</i>, <i>CSF1</i>, <i>CCL4</i>, <i>CCL2</i>, <i>CCL3</i>, <i>BCL2L1</i>, and <i>ITGB2</i>. Enrichment analysis of upregulated genes identified Gene Ontology Biological Processes related to cytokine responses and TNF-associated pathways. This study highlights α7nAChR activation as a key regulator of anti-inflammatory responses in BV2 microglia under OGDR conditions, with micro-RNA21 identified as a crucial mediator of receptor-driven neuroprotection via the TNF-α/NF<i>κ</i>B signalling pathway.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}