NeuroMolecular Medicine最新文献_第10页

Physical Exercise Inhibits Cognitive Impairment and Memory Loss in Aged Mice, and Enhances Pre- and Post-Synaptic Proteins in the Hippocampus of Young and Aged Mice. 体育锻炼可抑制老年小鼠的认知障碍和记忆丧失，并增强年轻小鼠和老年小鼠海马突触前后蛋白的功能

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-29 DOI: 10.1007/s12017-024-08798-x

Ricardo Augusto Leoni De Sousa, Caique Olegário Diniz-Magalhaes, Poliany Pereira Cruz, Gustavo Henrique Bahia de Oliveira, Julia Tereza Aparecida Caldeira Prates, Crisley Mara de Azevedo Ferreira, Rosiane Rosa Silva, Ricardo Cardoso Cassilhas

{"title":"Physical Exercise Inhibits Cognitive Impairment and Memory Loss in Aged Mice, and Enhances Pre- and Post-Synaptic Proteins in the Hippocampus of Young and Aged Mice.","authors":"Ricardo Augusto Leoni De Sousa, Caique Olegário Diniz-Magalhaes, Poliany Pereira Cruz, Gustavo Henrique Bahia de Oliveira, Julia Tereza Aparecida Caldeira Prates, Crisley Mara de Azevedo Ferreira, Rosiane Rosa Silva, Ricardo Cardoso Cassilhas","doi":"10.1007/s12017-024-08798-x","DOIUrl":"10.1007/s12017-024-08798-x","url":null,"abstract":"The aim of this study was to evaluate the effects of swimming in the brain and behavior of young and aged mice. Forty-eight male C57BL/6 J mice were randomly distributed into 4 groups (n = 12 per group, 3 and 18 months old). The subdivision of the groups was: 3 months-SED, 18 months-SED, 3 months-EXE, and 18 months-EXE. SED mice did not swim, while EXE mice performed the physical exercise protocol. Training was initiated 48 h after the adaptation week. Swimming sessions consisted of 30 min, with no overload, 5 days per week, for 4 weeks. After the exercise protocol, it was revealed working and spatial memory were impaired in the 18 months-SED group. Pre- and post-synaptic proteins were enhanced in the groups that swam when compared to the 3- and 8 months-SED groups. Lipid peroxidation was greater in the aged mice that did not perform the physical exercise protocol and might have contributed to the cognitive impairment in this group. In conclusion, an aerobic physical exercise protocol, performed through regular swimming sessions, inhibited cognitive impairment, memory loss and lipid peroxidation in the aged mice, while pre- and post-synaptic proteins were enhanced in the hippocampus of young and aged mice.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"31"},"PeriodicalIF":3.9,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141788752","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}

引用次数: 0

The CD44s Isoform is a Potential Biomarker for Predicting Craniopharyngioma Recurrence in Children. CD44s异构体是预测儿童颅咽管瘤复发的潜在生物标记物

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-17 DOI: 10.1007/s12017-024-08797-y

K Bajdak-Rusinek, N Diak, E Gutmajster, A Fus-Kujawa, M Ciupińska, B Kalina-Faska, A Trybus, M Grajek, M Kalina, M Mandera

{"title":"The CD44s Isoform is a Potential Biomarker for Predicting Craniopharyngioma Recurrence in Children.","authors":"K Bajdak-Rusinek, N Diak, E Gutmajster, A Fus-Kujawa, M Ciupińska, B Kalina-Faska, A Trybus, M Grajek, M Kalina, M Mandera","doi":"10.1007/s12017-024-08797-y","DOIUrl":"10.1007/s12017-024-08797-y","url":null,"abstract":"Adamantinomatous craniopharyngioma (ACP) is an intracranial tumor considered partly malignant due to its ability to infiltrate surrounding structures and tendency to relapse despite radical resection. CD44 is a known stem cell marker in ACP and is upregulated in cell clusters of invasive ACP protrusions; however, the functions of its alternative splicing isoform variants, CD44s and CD44v1-10, have not yet been studied in terms of ACP recurrence, despite their confirmed roles in cancer development and progression. In this study, we first confirmed the difference in total CD44 expression between samples from patients who experienced relapse and those from patients who did not. Moreover, our findings showed that, in recurrent samples, the predominant isoform expressed was CD44s, which might indicate its significance in predicting ACP recurrence. The association between increased CD44 expression and recurrence may lead to the development of prognostic markers of ACP aggressiveness and relapse potential; however, further studies are needed to clarify the exact mechanism of CD44 expression.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"30"},"PeriodicalIF":3.9,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11254967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634111","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}

引用次数: 0

Astaxanthin Rescues Memory Impairments in Rats with Vascular Dementia by Protecting Against Neuronal Death in the Hippocampus. 虾青素通过防止海马区神经元死亡修复血管性痴呆大鼠的记忆损伤

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-16 DOI: 10.1007/s12017-024-08796-z

Na Wei, Luo-Man Zhang, Jing-Jing Xu, Sheng-Lei Li, Rui Xue, Sheng-Li Ma, Cai Li, Miao-Miao Sun, Kui-Sheng Chen

{"title":"Astaxanthin Rescues Memory Impairments in Rats with Vascular Dementia by Protecting Against Neuronal Death in the Hippocampus.","authors":"Na Wei, Luo-Man Zhang, Jing-Jing Xu, Sheng-Lei Li, Rui Xue, Sheng-Li Ma, Cai Li, Miao-Miao Sun, Kui-Sheng Chen","doi":"10.1007/s12017-024-08796-z","DOIUrl":"10.1007/s12017-024-08796-z","url":null,"abstract":"Vascular dementia (VaD) is a cognitive disorder characterized by a decline in cognitive function resulting from cerebrovascular disease. The hippocampus is particularly susceptible to ischemic insults, leading to memory deficits in VaD. Astaxanthin (AST) has shown potential therapeutic effects in neurodegenerative diseases. However, the mechanisms underlying its protective effects in VaD and against hippocampal neuronal death remain unclear. In this study, We used the bilateral common carotid artery occlusion (BCCAO) method to establish a chronic cerebral hypoperfusion (CCH) rat model of VaD and administered a gastric infusion of AST at 25 mg/kg per day for 4 weeks to explore its therapeutic effects. Memory impairments were assessed using Y-maze and Morris water maze tests. We also performed biochemical analyses to evaluate levels of hippocampal neuronal death and apoptosis-related proteins, as well as the impact of astaxanthin on the PI3K/Akt/mTOR pathway and oxidative stress. Our results demonstrated that AST significantly rescued memory impairments in VaD rats. Furthermore, astaxanthin treatment protected against hippocampal neuronal death and attenuated apoptosis. We also observed that AST modulated the PI3K/Akt/mTOR pathway, suggesting its involvement in promoting neuronal survival and synaptic plasticity. Additionally, AST exhibited antioxidant properties, mitigating oxidative stress in the hippocampus. These findings provide valuable insights into the potential therapeutic effects of AST in VaD. By elucidating the mechanisms underlying the actions of AST, this study highlights the importance of protecting hippocampal neurons and suggests potential targets for intervention in VaD. There are still some unanswered questions include long-term effects and optimal dosage of the use in human. Further research is warranted to fully understand the therapeutic potential of AST and its application in the clinical treatment of VaD.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"29"},"PeriodicalIF":3.9,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627174","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}

引用次数: 0

A Comprehensive Overview of NF1 Mutations in Iranian Patients. 伊朗患者 NF1 基因突变综述

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-07-02 DOI: 10.1007/s12017-024-08790-5

Shahram Savad, Mohammad-Hossein Modarressi, Sarang Younesi, Mahnaz Seifi-Alan, Niusha Samadaian, Mona Masoomy, Mehdi Dianatpour, Shima Norouzi, Saloomeh Amidi, Amirreza Boroumand, Mahmoud Reza Ashrafi, Alireza Ronagh, Maryam Eslami, Maryam Hashemnejad, Shahab Nourian, Sanaz Mohammadi, Mohammad Mahdi Taheri Amin, Morteza Heidari, Mahin Seifi-Alan, Hossein Shojaaldini Ardakani, Fatemeh Aghamahdi, Sheyda Khalilian, Soudeh Ghafouri-Fard

{"title":"A Comprehensive Overview of NF1 Mutations in Iranian Patients.","authors":"Shahram Savad, Mohammad-Hossein Modarressi, Sarang Younesi, Mahnaz Seifi-Alan, Niusha Samadaian, Mona Masoomy, Mehdi Dianatpour, Shima Norouzi, Saloomeh Amidi, Amirreza Boroumand, Mahmoud Reza Ashrafi, Alireza Ronagh, Maryam Eslami, Maryam Hashemnejad, Shahab Nourian, Sanaz Mohammadi, Mohammad Mahdi Taheri Amin, Morteza Heidari, Mahin Seifi-Alan, Hossein Shojaaldini Ardakani, Fatemeh Aghamahdi, Sheyda Khalilian, Soudeh Ghafouri-Fard","doi":"10.1007/s12017-024-08790-5","DOIUrl":"10.1007/s12017-024-08790-5","url":null,"abstract":"Neurofibromatosis type 1 (NF1) is a genetic disorder caused by mutations in the NF1 gene. This disorder shows nearly complete penetrance and high phenotypic variability. We used the whole-exome sequencing technique to identify mutations in 32 NF1 cases from 22 Iranian families. A total of 31 variants, including 30 point mutations and one large deletion, were detected. In eight cases, variants were inherited, while they were sporadic in the remaining. Seven novel variants, including c.5576 T > G, c.6658_6659insC, c.2322dupT, c.92_93insAA, c.4360C > T, c.3814C > T, and c.4565_4566delinsC, were identified. The current study is the largest in terms of the sample size of Iranian NF1 cases with identified mutations. The results can broaden the spectrum of NF1 mutations and facilitate the process of genetic counseling in the affected families.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"28"},"PeriodicalIF":3.9,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492853","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}

引用次数: 0

Association of NID2 SNPs with Glioma Risk and Prognosis in the Chinese Population. 中国人群中 NID2 SNPs 与胶质瘤风险和预后的关系

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-27 DOI: 10.1007/s12017-024-08795-0

Jie Hao, Congmei Huang, Weiwei Zhao, Lin Zhao, Xiuxia Hu, WenJie Zhang, Le Guo, Xia Dou, Tianbo Jin, Mingjun Hu

{"title":"Association of NID2 SNPs with Glioma Risk and Prognosis in the Chinese Population.","authors":"Jie Hao, Congmei Huang, Weiwei Zhao, Lin Zhao, Xiuxia Hu, WenJie Zhang, Le Guo, Xia Dou, Tianbo Jin, Mingjun Hu","doi":"10.1007/s12017-024-08795-0","DOIUrl":"10.1007/s12017-024-08795-0","url":null,"abstract":"Glioma is the most common primary intracranial tumor with high mortality and poor prognosis. The purpose of this study was to investigate how single-nucleotide polymorphisms (SNPs) of the NID2 gene affect glioma risk and prognosis. Four candidate SNPs of NID2 in 529 glioma patients and 478 healthy controls were successfully genotyped by Agena MassARRAY mass spectrometer. Logistic regression was utilized to assess the associations between NID2 SNPs and glioma risk under different genetic models. Furthermore, the relationship between risk-related SNPs in NID2 and the prognosis of glioma patients was explored through Kaplan-Meier (KM) survival curve and Cox proportional hazard regression analysis. The results showed that rs11846847 (OR 1.24, p = 0.017) and rs1874569 (OR 1.22, p = 0.026) were significantly associated with an increased risk of glioma, and rs11846847 also had a risk-increasing effect on glioma in participants ≤ 40 years old. The interaction model of rs11846847 and rs1874569 could be more suitable for forecasting glioma risk. We also discovered a significant association between rs1874569 and poor prognosis in glioma patients (HR 1.32, p = 0.039) and especially CC genotype was relevant to shorter overall survival (OS) and progression-free survival (PFS) in patients with high-grade glioma. Additionally, the study demonstrated that gross total resection or chemotherapy improve glioma prognosis in the Chinese Han population. This study is the first to provide evidence for the association of NID2 SNPs with glioma risk and prognosis, suggesting that NID2 variants might be potential factors for glioma.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"27"},"PeriodicalIF":3.9,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141458346","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}

引用次数: 0

Hydrogen Sulfide can Scavenge Free Radicals to Improve Spinal Cord Injury by Inhibiting the p38MAPK/mTOR/NF-κB Signaling Pathway. 硫化氢可清除自由基，通过抑制 p38MAPK/mTOR/NF-κB 信号通路改善脊髓损伤。

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-21 DOI: 10.1007/s12017-024-08794-1

Kexin Lin, Yong Zhang, Yanyang Shen, Yiqin Xu, Min Huang, Xuehong Liu

引用次数: 0

FMOD Alleviates Depression-Like Behaviors by Targeting the PI3K/AKT/mTOR Signaling After Traumatic Brain Injury. FMOD通过靶向创伤性脑损伤后的PI3K/AKT/mTOR信号传导缓解抑郁行为

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-12 DOI: 10.1007/s12017-024-08793-2

Xuekang Huang, Ziyu Zhu, Mengran Du, Chenrui Wu, Jiayuanyuan Fu, Jie Zhang, Weilin Tan, Biying Wu, Lian Liu, Z B Liao

{"title":"FMOD Alleviates Depression-Like Behaviors by Targeting the PI3K/AKT/mTOR Signaling After Traumatic Brain Injury.","authors":"Xuekang Huang, Ziyu Zhu, Mengran Du, Chenrui Wu, Jiayuanyuan Fu, Jie Zhang, Weilin Tan, Biying Wu, Lian Liu, Z B Liao","doi":"10.1007/s12017-024-08793-2","DOIUrl":"10.1007/s12017-024-08793-2","url":null,"abstract":"Depression frequently occurs following traumatic brain injury (TBI). However, the role of Fibromodulin (FMOD) in TBI-related depression is not yet clear. Previous studies have suggested FMOD as a potential key factor in TBI, yet its association with depression post-TBI and underlying mechanisms are not well understood. Serum levels of FMOD were measured in patients with traumatic brain injury using qPCR. The severity of depression was assessed using the self-depression scale (SDS). Neurological function, depressive state, and cognitive function in mice were assessed using the modified Neurological Severity Score (mNSS), forced swimming test (FST), tail suspension test (TST), Sucrose Preference Test (SPT), and morris water maze (MWM). The morphological features of mouse hippocampal synapses and neuronal dendritic spines were revealed through immunofluorescence, transmission electron microscopy, and Golgi-Cox staining. The protein expression levels of FMOD, MAP2, SYP, and PSD95, as well as the phosphorylation levels of the PI3K/AKT/mTOR signaling pathway, were detected through Western blotting. FMOD levels were decreased in TBI patients' serum. Overexpression of FMOD preserved neuronal function and alleviated depression-like behaviour, increased synaptic protein expression, and induced ultrastructural changes in hippocampal neurons. The increased phosphorylation of PI3K, AKT, and mTOR suggested the involvement of the PI3K/AKT/mTOR signaling pathway in FMOD's protective effects. FMOD exhibits potential as a therapeutic target for depression related to TBI, with its protective effects potentially mediated through the PI3K/AKT/mTOR signaling pathway.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"24"},"PeriodicalIF":3.9,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11169026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306476","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}

引用次数: 0

Protein Disulfide Isomerase Endoplasmic Reticulum Protein 57 (ERp57) is Protective Against ALS-Associated Mutant TDP-43 in Neuronal Cells. 蛋白二硫化物同工酶内质网蛋白 57 (ERp57) 对神经元细胞中与 ALS 相关的突变 TDP-43 有保护作用。

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-11 DOI: 10.1007/s12017-024-08787-0

Sonam Parakh, Emma R Perri, Marta Vidal, Zeinab Takalloo, Cyril J Jagaraj, Prachi Mehta, Shu Yang, Colleen J Thomas, Ian P Blair, Yuning Hong, Julie D Atkin

{"title":"Protein Disulfide Isomerase Endoplasmic Reticulum Protein 57 (ERp57) is Protective Against ALS-Associated Mutant TDP-43 in Neuronal Cells.","authors":"Sonam Parakh, Emma R Perri, Marta Vidal, Zeinab Takalloo, Cyril J Jagaraj, Prachi Mehta, Shu Yang, Colleen J Thomas, Ian P Blair, Yuning Hong, Julie D Atkin","doi":"10.1007/s12017-024-08787-0","DOIUrl":"10.1007/s12017-024-08787-0","url":null,"abstract":"Amyotrophic Lateral Sclerosis (ALS) is a severe neurodegenerative disease affecting motor neurons. Pathological forms of Tar-DNA binding protein-43 (TDP-43), involving its mislocalisation to the cytoplasm and the formation of misfolded inclusions, are present in almost all ALS cases (97%), and ~ 50% cases of the related condition, frontotemporal dementia (FTD), highlighting its importance in neurodegeneration. Previous studies have shown that endoplasmic reticulum protein 57 (ERp57), a member of the protein disulphide isomerase (PDI) family of redox chaperones, is protective against ALS-linked mutant superoxide dismutase (SOD1) in neuronal cells and transgenic SOD1G93A mouse models. However, it remains unclear whether ERp57 is protective against pathological TDP-43 in ALS. Here, we demonstrate that ERp57 is protective against key features of TDP-43 pathology in neuronal cells. ERp57 inhibited the mislocalisation of TDP-43M337V from the nucleus to the cytoplasm. In addition, ERp57 inhibited the number of inclusions formed by ALS-associated variant TDP-43M337V and reduced the size of these inclusions. ERp57 was also protective against ER stress and induction of apoptosis. Furthermore, ERp57 modulated the steady-state expression levels of TDP-43. This study therefore demonstrates a novel mechanism of action of ERp57 in ALS. It also implies that ERp57 may have potential as a novel therapeutic target to prevent the TDP-43 pathology associated with neurodegeneration.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"23"},"PeriodicalIF":3.9,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11166824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141301134","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}

引用次数: 0

p39 Affects Myelin Formation in Cerebral Ischemic Injury. p39 影响脑缺血损伤中髓鞘的形成

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-06-01 DOI: 10.1007/s12017-024-08792-3

Danyang Meng, Di Wu, Xiaojing Li, Zhigang Miao

引用次数: 0

Influence of SLC40A1 on Cytokine Interactions and Immune Infiltration in Glioblastoma. SLC40A1 对胶质母细胞瘤中细胞因子相互作用和免疫渗透的影响

IF 3.9 4区医学

NeuroMolecular Medicine Pub Date : 2024-05-16 DOI: 10.1007/s12017-024-08789-y

Jiahao Jiang, Riquan Duan, Junle Zhu, Junqing Yan, Jingliang Ye, Chun Luo

{"title":"Influence of SLC40A1 on Cytokine Interactions and Immune Infiltration in Glioblastoma.","authors":"Jiahao Jiang, Riquan Duan, Junle Zhu, Junqing Yan, Jingliang Ye, Chun Luo","doi":"10.1007/s12017-024-08789-y","DOIUrl":"10.1007/s12017-024-08789-y","url":null,"abstract":"Numerous studies have explored the various functions of Slc40a1 in cancer development. However, the role of Slc40a1 in primary glioblastoma requires further investigation. Initially, we observed that GBM patients with high Slc40a1 expression had a more favorable prognosis than those with low Slc40a1 expression, as evidenced by an analysis of the TIMER database. Subsequent analysis using the cancer genome atlas (TCGA) database enabled us to identify potential underlying mechanisms involved. Further analyses, including GO, KEGG, GSEA, immune infiltration, and correlation analyses, revealed that Slc40a1 primarily affected cytokine interactions, particularly with Ccl14 and Il18, resulting in changes in the immune microenvironment and ultimately leading to a better prognosis in GBM patients. We validated our findings by examining a tissue microarray with 180 samples and confirmed that GBM patients with high SLC40A1 protein expression exhibited more favorable prognostic outcomes than those with low SLC40A1 protein expression. Immunofluorescence analysis also revealed a significant correlation between SLC40A1 protein expression and the protein expression of IL18 and CCL14. These findings suggest that Slc40a1 may play a role in GBM pathogenesis by modulating the tumor immune microenvironment through the regulation of Il18 and Ccl14. Hence, targeting Slc40a1 might offer potential benefits for immunotherapeutic interventions and prognostic assessments in GBM patients.","PeriodicalId":19304,"journal":{"name":"NeuroMolecular Medicine","volume":"26 1","pages":"21"},"PeriodicalIF":3.9,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140945529","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}

引用次数: 0