Molecular Neurobiology最新文献

筛选
英文 中文
Oral Microbiota and Porphyromonas gingivalis Kgp Genotypes Altered in Parkinson's Disease with Mild Cognitive Impairment. 帕金森病伴轻度认知障碍患者的口腔微生物群和牙龈卟啉单胞菌 Kgp 基因型发生改变
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-03-27 DOI: 10.1007/s12035-024-04119-2
Dongcheng Li, Tengzhu Ren, Hao Li, Mingdi Huang, Jiaxin Chen, Qishan He, Wei Lv, Hailing Liu, Renshi Xu, Xiong Zhang
{"title":"Oral Microbiota and Porphyromonas gingivalis Kgp Genotypes Altered in Parkinson's Disease with Mild Cognitive Impairment.","authors":"Dongcheng Li, Tengzhu Ren, Hao Li, Mingdi Huang, Jiaxin Chen, Qishan He, Wei Lv, Hailing Liu, Renshi Xu, Xiong Zhang","doi":"10.1007/s12035-024-04119-2","DOIUrl":"10.1007/s12035-024-04119-2","url":null,"abstract":"<p><p>Cognitive impairment (CI) is a common complication of the non-motor symptoms in Parkinson's disease (PD), including PD with mild cognitive impairment (PD-MCI) and PD dementia. Recent studies reported the oral dysbiosis in PD and CI, respectively. Porphyromonas gingivalis (P. gingivalis), a pathogen of oral dysbiosis, plays an important role in PD, whose lysine-gingipain (Kgp) could lead to AD-type pathologies. No previous study investigated the composition of oral microbiota and role of P. gingivalis in PD-MCI. This study aimed to investigate the differences of oral microbiota composition, P. gingivalis copy number, and Kgp genotypes among PD-MCI, PD with normal cognition (PD-NC) and periodontal status-matched control (PC) groups. The oral bacteria composition, the copy number of P. gingivalis, and the Kgp genotypes in gingival crevicular fluid from PD-MCI, PD-NC, and PC were analyzed using 16S ribosomal RNA sequencing, quantitative real-time PCR, and MseI restriction. We found that the structures of oral microbiota in PD-MCI group were significantly different compared to that in PD-NC and PC group. The relative abundances of Prevotella, Lactobacillus, Megasphaera, Atopobium, and Howardella were negatively correlated with cognitive score. Moreover, there was a significant difference of Kgp genotypes among the three groups. The predominant Kgp genotypes of P. gingivalis in the PD-MCI group were primarily Kgp II, whereas in the PD-NC group, it was mainly Kgp I. The Kgp II correlated with lower MMSE and MoCA scores, which suggested that Kgp genotypes II is related to cognitive impairment in PD.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140306156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Oligomeric Amyloid-β and Tau Alter Cell Adhesion Properties and Induce Inflammatory Responses in Cerebral Endothelial Cells Through the RhoA/ROCK Pathway. 寡聚淀粉样蛋白-β和Tau通过RhoA/ROCK途径改变细胞粘附特性并诱导脑内皮细胞的炎症反应
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-04-02 DOI: 10.1007/s12035-024-04138-z
Faruk Hossen, Xue Geng, Grace Y Sun, Xincheng Yao, James C Lee
{"title":"Oligomeric Amyloid-β and Tau Alter Cell Adhesion Properties and Induce Inflammatory Responses in Cerebral Endothelial Cells Through the RhoA/ROCK Pathway.","authors":"Faruk Hossen, Xue Geng, Grace Y Sun, Xincheng Yao, James C Lee","doi":"10.1007/s12035-024-04138-z","DOIUrl":"10.1007/s12035-024-04138-z","url":null,"abstract":"<p><p>Dysfunction of cerebral endothelial cells (CECs) has been implicated in the pathology of Alzheimer's disease (AD). Despite evidence showing cytotoxic effects of oligomeric amyloid-β (oAβ) and Tau (oTau) in the central nervous system, their direct effects on CECs have not been fully investigated. In this study, we examined the direct effects of oAβ, oTau, and their combination on cell adhesion properties and inflammatory responses in CECs. We found that both oAβ and oTau increased cell stiffness, as well as the p-selectin/Sialyl-Lewis<sup>X</sup> (sLe<sup>X</sup>) bonding-mediated membrane tether force and probability of adhesion in CECs. Consistent with these biomechanical alterations, treatments with oAβ or oTau also increased actin polymerization and the expression of p-selectin at the cell surface. These toxic oligomeric peptides also triggered inflammatory responses, including upregulations of p-NF-kB p65, IL-1β, and TNF-α. In addition, they rapidly activated the RhoA/ROCK pathway. These biochemical and biomechanical changes were further enhanced by the treatment with the combination of oAβ and oTau, which were significantly suppressed by Fasudil, a specific inhibitor for the RhoA/ROCK pathway. In conclusion, our data suggest that oAβ, oTau, and their combination triggered subcellular mechanical alterations and inflammatory responses in CECs through the RhoA/ROCK pathway.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140336235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
OTULIN Can Improve Spinal Cord Injury by the NF-κB and Wnt/β-Catenin Signaling Pathways. OTULIN 可通过 NF-κB 和 Wnt/β-Catenin 信号通路改善脊髓损伤。
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-04-02 DOI: 10.1007/s12035-024-04134-3
Qianhui Wang, Lvxia Wang, Benson O A Botchway, Yong Zhang, Min Huang, Xuehong Liu
{"title":"OTULIN Can Improve Spinal Cord Injury by the NF-κB and Wnt/β-Catenin Signaling Pathways.","authors":"Qianhui Wang, Lvxia Wang, Benson O A Botchway, Yong Zhang, Min Huang, Xuehong Liu","doi":"10.1007/s12035-024-04134-3","DOIUrl":"10.1007/s12035-024-04134-3","url":null,"abstract":"<p><p>Spinal cord injury (SCI) is a significant health concern, as it presently has no effective treatment in the clinical setting. Inflammation is a key player in the pathophysiological process of SCI, with a number of studies evidencing that the inhibition of the NF-κB signaling pathway may impede the inflammatory response and improve SCI. OTULIN, as a de-ubiquitination enzyme, the most notable is its anti-inflammatory effect. OTULIN can inhibit the NF-κB signaling pathway to suppress the inflammatory reaction via de-ubiquitination. In addition, OTULIN may promote vascular regeneration through the Wnt/β-catenin pathway in the wake of SCI. In this review, we analyze the structure and physiological function of OTULIN, along with both NF-κB and Wnt/β-catenin signaling pathways. Furthermore, we examine the significant role of OTULIN in SCI through its impairment of the NF-κB signaling pathway, which could open the possibility of it being a novel interventional target for the condition.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140336236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Circ-Bptf Ameliorates Learning and Memory Impairments via the miR-138-5p/p62 Axis in APP/PS1 Mice. Circ-Bptf通过miR-138-5p/p62轴改善APP/PS1小鼠的学习和记忆障碍
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-03-25 DOI: 10.1007/s12035-024-04066-y
Hong-Fang Wang, Yi-Bo Li, Zi-Yu Liu, Wen-Meng Xie, Qing Liu, Run-Jiao Zhang, Wen-Yu Wang, Jia-Xin Hao, Lei Wang, Dan-Dan Geng
{"title":"Circ-Bptf Ameliorates Learning and Memory Impairments via the miR-138-5p/p62 Axis in APP/PS1 Mice.","authors":"Hong-Fang Wang, Yi-Bo Li, Zi-Yu Liu, Wen-Meng Xie, Qing Liu, Run-Jiao Zhang, Wen-Yu Wang, Jia-Xin Hao, Lei Wang, Dan-Dan Geng","doi":"10.1007/s12035-024-04066-y","DOIUrl":"10.1007/s12035-024-04066-y","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a common age-associated progressive neurodegenerative disorder that is implicated in the aberrant regulation of numerous circular RNAs (circRNAs). Here, we reported that circ-Bptf, a conserved circRNA derived from the Bptf gene, showed an age-dependent decrease in the hippocampus of APP/PS1 mice. Overexpression of circ-Bptf significantly reversed dendritic spine loss and learning and memory impairment in APP/PS1 mice. Moreover, we found that circ-Bptf was predominantly localized to the cytoplasm and upregulated p62 expression by binding to miR-138-5p. Furthermore, the miR-138-5p mimics reversed the decreased expression of p62 induced by the silencing of circ-Bptf. Together, our findings suggested that circ-Bptf ameliorated learning and memory impairments via the miR-138-5p/p62 axis in APP/PS1 mice. It may act as a potential player in AD pathogenesis and therapy.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140288555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
EZH2 Promotes Glioma Cell Proliferation, Invasion, and Migration via Mir-142-3p/KCNQ1OT1/HMGB3 Axis : Running Title: EZH2 Promotes Glioma cell Malignant Behaviors. EZH2 通过 Mir-142-3p/KCNQ1OT1/HMGB3 轴促进胶质瘤细胞增殖、侵袭和迁移 :运行标题:EZH2 促进胶质瘤细胞恶性行为。
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-04-01 DOI: 10.1007/s12035-024-04080-0
Yiming Zhang, Yong Yu, Lei Yuan, Baozhong Zhang
{"title":"EZH2 Promotes Glioma Cell Proliferation, Invasion, and Migration via Mir-142-3p/KCNQ1OT1/HMGB3 Axis : Running Title: EZH2 Promotes Glioma cell Malignant Behaviors.","authors":"Yiming Zhang, Yong Yu, Lei Yuan, Baozhong Zhang","doi":"10.1007/s12035-024-04080-0","DOIUrl":"10.1007/s12035-024-04080-0","url":null,"abstract":"<p><p>This study investigates the role and molecular mechanism of EZH2 in glioma cell proliferation, invasion, and migration. EZH2, miR-142-3p, lncRNA KCNQ1OT1, LIN28B, and HMGB3 expressions in glioma tissues and cells were determined using qRT-PCR or Western blot, followed by CCK-8 assay detection of cell viability, Transwell detection of invasion and migration, ChIP analysis of the enrichment of EZH2 and H3K27me3 on miR-142-3p promoter, dual-luciferase reporter assay and RIP validation of the binding of miR-142-3p-KCNQ1OT1 and KCNQ1OT1-LIN28B, and actinomycin D detection of KCNQ1OT1 and HMGB3 mRNA stability. A nude mouse xenograft model and a lung metastasis model were established. EZH2, KCNQ1OT1, LIN28B, and HMGB3 were highly expressed while miR-142-3p was poorly expressed in gliomas. EZH2 silencing restrained glioma cell proliferation, invasion, and migration. EZH2 repressed miR-142-3p expression by elevating the H3K27me3 level. miR-142-3p targeted KCNQ1OT1 expression, and KCNQ1OT1 bound to LIN28B to stabilize HMGB3 mRNA, thereby promoting its protein expression. EZH2 silencing depressed tumor growth and metastasis in nude mice via the miR-142-3p/KCNQ1OT1/HMGB3 axis. In conclusion, EZH2 curbed miR-142-3p expression, thereby relieving the inhibition of KCNQ1OT1 expression by miR-142-3p, enhancing the binding of KCNQ1OT1 to LIN28B, elevating HMGB3 expression, and ultimately accelerating glioma cell proliferation, invasion, and migration.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140331925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Receptor-Assisted Nanotherapeutics for Overcoming the Blood-Brain Barrier. 用于克服血脑屏障的受体辅助纳米疗法。
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-04-01 DOI: 10.1007/s12035-024-04015-9
Akshada Mhaske, Shalini Shukla, Kailash Ahirwar, Kamalinder K Singh, Rahul Shukla
{"title":"Receptor-Assisted Nanotherapeutics for Overcoming the Blood-Brain Barrier.","authors":"Akshada Mhaske, Shalini Shukla, Kailash Ahirwar, Kamalinder K Singh, Rahul Shukla","doi":"10.1007/s12035-024-04015-9","DOIUrl":"10.1007/s12035-024-04015-9","url":null,"abstract":"<p><p>Blood-brain barrier (BBB) is a distinguishing checkpoint that segregates peripheral organs from neural compartment. It protects the central nervous system from harmful ambush of antigens and pathogens. Owing to such explicit selectivity, the BBB hinders passage of various neuroprotective drug molecules that escalates into poor attainability of neuroprotective agents towards the brain. However, few molecules can surpass the BBB and gain access in the brain parenchyma by exploiting surface transporters and receptors. For successful development of brain-targeted therapy, understanding of BBB transporters and receptors is crucial. This review focuses on the transporter and receptor-based mechanistic pathway that can be manoeuvred for better comprehension of reciprocity of receptors and nanotechnological vehicle delivery. Nanotechnology has emerged as one of the expedient noninvasive approaches for brain targeting via manipulating the hurdle of the BBB. Various nanovehicles are being reported for brain-targeted delivery such as nanoparticles, nanocrystals, nanoemulsion, nanolipid carriers, liposomes and other nanovesicles. Nanotechnology-aided brain targeting can be a strategic approach to circumvent the BBB without altering the inherent nature of the BBB.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140336237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Identification of Anoikis-Related Genes in Spinal Cord Injury: Bioinformatics and Experimental Validation. 脊髓损伤中与 Anoikis 相关基因的鉴定:生物信息学和实验验证。
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-03-23 DOI: 10.1007/s12035-024-04121-8
Wen Yin, Zhipeng Jiang, Youwei Guo, Yudong Cao, Zhaoping Wu, Yi Zhou, Quan Chen, Weidong Liu, Xingjun Jiang, Caiping Ren
{"title":"Identification of Anoikis-Related Genes in Spinal Cord Injury: Bioinformatics and Experimental Validation.","authors":"Wen Yin, Zhipeng Jiang, Youwei Guo, Yudong Cao, Zhaoping Wu, Yi Zhou, Quan Chen, Weidong Liu, Xingjun Jiang, Caiping Ren","doi":"10.1007/s12035-024-04121-8","DOIUrl":"10.1007/s12035-024-04121-8","url":null,"abstract":"<p><p>Spinal cord injury (SCI) is a serious disease without effective therapeutic strategies. To identify the potential treatments for SCI, it is extremely important to explore the underlying mechanism. Current studies demonstrate that anoikis might play an important role in SCI. In this study, we aimed to identify the key anoikis-related genes (ARGs) providing therapeutic targets for SCI. The mRNA expression matrix of GSE45006 was downloaded from the Gene Expression Omnibus (GEO) database, and the ARGs were downloaded from the Molecular Signatures Database (MSigDB database). Then, the potential differentially expressed ARGs were identified. Next, correlation analysis, gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and protein-protein interaction (PPI) analysis were employed for the differentially expressed ARGs. Moreover, miRNA-gene networks were constructed by the hub ARGs. Finally, RNA expression of the top ten hub ARGs was validated in the SCI cell model and rat SCI model. A total of 27 common differentially expressed ARGs were identified at different time points (1, 3, 7, and 14 days) following SCI. The GO and KEGG enrichment analysis of these ARGs indicated several enriched terms related to proliferation, cell cycle, and apoptotic process. The PPI results revealed that most of the ARGs interacted with each other. Ten hub ARGs were further screened, and all the 10 genes were validated in the SCI cell model. In the rat model, only seven genes were validated eventually. We identified 27 differentially expressed ARGs of the SCI through bioinformatic analysis. Seven real hub ARGs (CCND1, FN1, IGF1, MYC, STAT3, TGFB1, and TP53) were identified eventually. These results may expand our understanding of SCI and contribute to the exploration of potential SCI targets.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140194180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Biochemical, Biomarker, and Behavioral Characterization of the GrnR493X Mouse Model of Frontotemporal Dementia. GrnR493X额颞叶痴呆小鼠模型的生化、生物标记和行为特征。
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-05-02 DOI: 10.1007/s12035-024-04190-9
Denise M Smith, Geetika Aggarwal, Michael L Niehoff, Spencer A Jones, Subhashis Banerjee, Susan A Farr, Andrew D Nguyen
{"title":"Biochemical, Biomarker, and Behavioral Characterization of the Grn<sup>R493X</sup> Mouse Model of Frontotemporal Dementia.","authors":"Denise M Smith, Geetika Aggarwal, Michael L Niehoff, Spencer A Jones, Subhashis Banerjee, Susan A Farr, Andrew D Nguyen","doi":"10.1007/s12035-024-04190-9","DOIUrl":"10.1007/s12035-024-04190-9","url":null,"abstract":"<p><p>Heterozygous loss-of-function mutations in the progranulin gene (GRN) are a major cause of frontotemporal dementia due to progranulin haploinsufficiency; complete deficiency of progranulin causes neuronal ceroid lipofuscinosis. Several progranulin-deficient mouse models have been generated, including both knockout mice and knockin mice harboring a common patient mutation (R493X). However, the Grn<sup>R493X</sup> mouse model has not been characterized completely. Additionally, while homozygous Grn<sup>R493X</sup> and Grn knockout mice have been extensively studied, data from heterozygous mice is still limited. Here, we performed more in-depth characterization of heterozygous and homozygous Grn<sup>R493X</sup> knockin mice, which includes biochemical assessments, behavioral studies, and analysis of fluid biomarkers. In the brains of homozygous Grn<sup>R493X</sup> mice, we found increased phosphorylated TDP-43 along with increased expression of lysosomal genes, markers of microgliosis and astrogliosis, pro-inflammatory cytokines, and complement factors. Heterozygous Grn<sup>R493X</sup> mice did not have increased TDP-43 phosphorylation but did exhibit limited increases in lysosomal and inflammatory gene expression. Behavioral studies found social and emotional deficits in Grn<sup>R493X</sup> mice that mirror those observed in Grn knockout mouse models, as well as impairment in memory and executive function. Overall, the Grn<sup>R493X</sup> knockin mouse model closely phenocopies Grn knockout models. Lastly, in contrast to homozygous knockin mice, heterozygous Grn<sup>R493X</sup> mice do not have elevated levels of fluid biomarkers previously identified in humans, including neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) in both plasma and CSF. These results may help to inform pre-clinical studies that use this Grn knockin mouse model and other Grn knockout models.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140859765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Utilizing Machine Learning to Identify Biomarkers of Endoplasmic Reticulum Stress and Analyze Immune Cell Infiltration in Parkinson's Disease. 利用机器学习识别内质网应激的生物标记物并分析帕金森病的免疫细胞浸润。
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-03-23 DOI: 10.1007/s12035-024-03948-5
Guang Yang, Bing Zhang, Chun Yang Xu, Jia Wen Wu, Yi Zhang, Yue Yu, Xiao Gang He, Jun Dou
{"title":"Utilizing Machine Learning to Identify Biomarkers of Endoplasmic Reticulum Stress and Analyze Immune Cell Infiltration in Parkinson's Disease.","authors":"Guang Yang, Bing Zhang, Chun Yang Xu, Jia Wen Wu, Yi Zhang, Yue Yu, Xiao Gang He, Jun Dou","doi":"10.1007/s12035-024-03948-5","DOIUrl":"10.1007/s12035-024-03948-5","url":null,"abstract":"<p><p>The neurodegenerative disorder known as Parkinson's disease (PD) affects many people. The objective of this investigation was to examine the relationship between immune system infiltration, ATP-binding cassette transporter subfamily A member 7 (ABCA7) and TBL2 as well as potential therapeutic targets for the identification of PD associated to endoplasmic reticulum (ER) stress. First, we obtained PD data through GEO and divided it into two sets: a training set (GSE8397) plus a set for validation (GSE7621). Functional enrichment analysis was performed on a set of DEGs that overlapped with genes involved in endoplasmic reticulum stress. To identify genes of PD linked with endoplasmic reticulum stress, we employed random forest (RF) along with the least absolute shrinkage and selection operator (LASSO) logistic regression. Spearman's rank correlation analysis was then used to find associations among diagnostic markers with immune cell penetration. A grand total of 2 stress-related endoplasmic reticulum signature transcripts were identified. ABCA7 and TBL2 were shown to have diagnostic potential for PD and immune infiltrating cells have a role in the etiology of the disease. Additionally, resting CD4 memory, plasma cells, and NK cells overall exhibited positive associations with ABCA7, whereas triggered macrophages, T cells with active CD4 memory, activating NK cells, T cells with activated CD4 naive, engaged NK cells, and neutrophils all had adverse interactions with ABCA7. Overall, ABCA7 together with TBL2 have diagnostic utility for PD, and several types of immune cells, especially macrophages, may be involved in the development and progression of the disease.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140194183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Causal Relationships Between Gut Microbiota, Inflammatory Cells/Proteins, and Subarachnoid Hemorrhage: A Multi-omics Bidirectional Mendelian Randomization Study and Meta-analysis. 肠道微生物群、炎症细胞/蛋白与蛛网膜下腔出血之间的因果关系:多组学双向孟德尔随机化研究与 Meta 分析》(A Multi-omics Bidirectional Mendelian Randomization Study and Meta-analysis.
IF 4.6 2区 医学
Molecular Neurobiology Pub Date : 2024-11-01 Epub Date: 2024-03-25 DOI: 10.1007/s12035-024-04101-y
Congzhi Yan, Yun Li
{"title":"Causal Relationships Between Gut Microbiota, Inflammatory Cells/Proteins, and Subarachnoid Hemorrhage: A Multi-omics Bidirectional Mendelian Randomization Study and Meta-analysis.","authors":"Congzhi Yan, Yun Li","doi":"10.1007/s12035-024-04101-y","DOIUrl":"10.1007/s12035-024-04101-y","url":null,"abstract":"<p><p>Subarachnoid hemorrhage (SAH) is a neurological emergency that can lead to fatal outcomes. It occurs when bleeding happens in the subarachnoid space, a small gap between the arachnoid and pia mater. This condition results from the rupture of diseased or damaged blood vessels at the brain's base or surface. This study combined various omics approaches with Mendelian randomization analysis, including MR-IVW, MR Egger, MR weight median, and MR weight mode, to generate preliminary results. It also employed reverse Mendelian randomization, treating SAH as the exposure. Finally, a meta-analysis was conducted to summarize these findings. The study found positive correlations between SAH and both GBPA-Pyridoxal 5 phosphate biosynthesis I (OR=1.48, 95% CI, 1.04-2.12) and GBPA-glucose biosynthesis I (OR=0.68, 95% CI, 0.52-0.90). Increased levels of urokinase-type plasma activator were also associated with SAH (OR=1.17, 95% CI, 1.04-1.32). Associations were observed with SAH for CD80 on CD62L+ plasmacytoid dendritic cells, CD80 on plasmacytoid dendritic cells, CD123 on CD62L+ plasmacytoid dendritic cells, and SSC-A on plasmacytoid dendritic cells. This study, through Mendelian randomization and meta-analysis, established links between SAH and four inflammatory cells, one inflammatory protein, and two gut microbiota-related pathways. These findings suggest potential treatment targets for SAH, highlighting the importance of modulating gut microbiota and utilizing anti-inflammatory drugs in its management.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140207212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信