115563
论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
- 3.6 Breast Cancer (Dove Med Press)
- 4.3 Clin Epidemiol
- 2.6 Cancer Manag Res
- 3.2 Infect Drug Resist
- 4.1 Clin Interv Aging
- 6.1 Drug Des Dev Ther
- 4.1 Int J Chronic Obstr
- 8.7 Int J Nanomed
- 2.5 Int J Women's Health
- 3.2 Neuropsych Dis Treat
- 2.4 OncoTargets Ther
- 2.6 Patient Prefer Adher
- 2.6 Ther Clin Risk Manag
- 3.1 J Pain Res
- 3.5 Diabet Metab Synd Ob
- 4.5 Psychol Res Behav Ma
- 3.4 Nat Sci Sleep
- 2.4 Pharmgenomics Pers Med
- 2.6 Risk Manag Healthc Policy
- 4.6 J Inflamm Res
- 2.3 Int J Gen Med
- 3.9 J Hepatocell Carcinoma
- 3.3 J Asthma Allergy
- 2.5 Clin Cosmet Investig Dermatol
- 3.0 J Multidiscip Healthc
已发表论文
整合多组学分析鉴定出 CD84 相关的小胶质细胞在局灶性皮质发育不良 II 型中的改变
Authors Fang Y , Yang S, Lei L, Li Y , Zhang Y, Huang T, Zhou L
Received 17 September 2025
Accepted for publication 16 December 2025
Published 8 January 2026 Volume 2026:19 566227
DOI https://doi.org/10.2147/JIR.S566227
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Ning Quan
Yubao Fang,* Shengyu Yang,* Lei Lei,* Yinchao Li, Yaqian Zhang, Tiancai Huang, Liemin Zhou
Department of Neurology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, Guangdong, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Liemin Zhou, Email zhoulm@mail.sysu.edu.cn
Background: Focal cortical dysplasia type II (FCDII) is a major cause of drug-resistant epilepsy in children, yet its molecular pathogenesis remains poorly characterized. Accumulating evidence has underscored the critical role of persistent neuroinflammatory activity in the pathogenesis of focal cortical dysplasia.
Methods: We employed an integrated multi-omics approach to dissect the molecular pathology of FCDII. This included data-independent acquisition mass spectrometry (DIA-MS) proteomics and re-analysis of public transcriptomic datasets. Differential expression analysis, protein-protein interaction (PPI) network construction, and hub gene identification were performed. Key findings were validated using quantitative real-time PCR (qPCR) and further investigated through analysis of single-cell RNA sequencing (scRNA-seq) data to resolve cellular heterogeneity and cell-cell communication.
Results: Proteomic profiling of FCDII tissue identified 460 differentially expressed proteins (DEPs) enriched in cortical development, cytoskeletal organization, and immune–inflammatory signaling. Protein–protein interaction (PPI) network analysis further prioritized several hub molecules, among which the pro-inflammatory glycoprotein CD84 exhibited consistent upregulation across both proteomic and transcriptomic datasets. Single-cell analysis revealed that CD84 expression was preferentially localized to a microglial subpopulation characterized exhibiting elevated inflammation-related signatures, with particularly prominent enrichment in FCDIIB samples. CD84-positive microglia also demonstrated increased predicted interactions with astrocytes, neurons, and endothelial cells through signaling pathways involving colony-stimulating factor (CSF), CX3C motif chemokine, macrophage migration inhibitory factor (MIF), and somatostatin-related signaling.
Conclusion: Our multi-omics approaches suggest a potential role for CD84 in influencing microglial inflammatory states and in shaping their predicted interactions with astrocytes, neurons, and endothelial cells in FCDII. These findings offer preliminary molecular clues that may inform future mechanistic investigations of microglial alterations in this disorder.
Keywords: focal cortical dysplasia type II, multi-omics integration, neuroinflammation, CD84, microglial activation
Department of Neurology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, Guangdong, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Liemin Zhou, Email zhoulm@mail.sysu.edu.cn
Background: Focal cortical dysplasia type II (FCDII) is a major cause of drug-resistant epilepsy in children, yet its molecular pathogenesis remains poorly characterized. Accumulating evidence has underscored the critical role of persistent neuroinflammatory activity in the pathogenesis of focal cortical dysplasia.
Methods: We employed an integrated multi-omics approach to dissect the molecular pathology of FCDII. This included data-independent acquisition mass spectrometry (DIA-MS) proteomics and re-analysis of public transcriptomic datasets. Differential expression analysis, protein-protein interaction (PPI) network construction, and hub gene identification were performed. Key findings were validated using quantitative real-time PCR (qPCR) and further investigated through analysis of single-cell RNA sequencing (scRNA-seq) data to resolve cellular heterogeneity and cell-cell communication.
Results: Proteomic profiling of FCDII tissue identified 460 differentially expressed proteins (DEPs) enriched in cortical development, cytoskeletal organization, and immune–inflammatory signaling. Protein–protein interaction (PPI) network analysis further prioritized several hub molecules, among which the pro-inflammatory glycoprotein CD84 exhibited consistent upregulation across both proteomic and transcriptomic datasets. Single-cell analysis revealed that CD84 expression was preferentially localized to a microglial subpopulation characterized exhibiting elevated inflammation-related signatures, with particularly prominent enrichment in FCDIIB samples. CD84-positive microglia also demonstrated increased predicted interactions with astrocytes, neurons, and endothelial cells through signaling pathways involving colony-stimulating factor (CSF), CX3C motif chemokine, macrophage migration inhibitory factor (MIF), and somatostatin-related signaling.
Conclusion: Our multi-omics approaches suggest a potential role for CD84 in influencing microglial inflammatory states and in shaping their predicted interactions with astrocytes, neurons, and endothelial cells in FCDII. These findings offer preliminary molecular clues that may inform future mechanistic investigations of microglial alterations in this disorder.
Keywords: focal cortical dysplasia type II, multi-omics integration, neuroinflammation, CD84, microglial activation