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识别缺血性中风中的焦亡核心基因和炎症细胞类型相关基因。

Identifying Pyroptosis-Hub Genes and Inflammation Cell Type-Related Genes in Ischemic Stroke.

作者信息

Ge Wei, Cao Liangbin, Liu Can, Wang Hao, Lu Meijing, Chen Yongquan, Wang Ye

机构信息

Department of Anesthesiology, Yijishan Hospital, First Affiliated Hospital of Wannan Medical College, Wuhu, 241004, China.

出版信息

Mol Neurobiol. 2025 May;62(5):6228-6255. doi: 10.1007/s12035-024-04647-x. Epub 2025 Jan 3.

DOI:10.1007/s12035-024-04647-x
PMID:39798044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11953102/
Abstract

Stroke is the second-leading global cause of death. The damage attributed to the immune storm triggered by ischemia-reperfusion injury (IRI) post-stroke is substantial. However, data on the transcriptomic dynamics of pyroptosis in IRI are limited. This study aimed to analyze the expression of key pyroptosis genes in stroke and their correlation with immune infiltration. Pyroptosis-related genes were identified from the obtained middle cerebral artery occlusion (MCAO) datasets. Differential expression and functional analyses of pyroptosis-related genes were performed, and differences in functional enrichment between high-risk and low-risk groups were determined. An MCAO diagnostic model was constructed and validated using selected pyroptosis-related genes with differential expression. High- and low-risk MCAO groups were constructed for expression and immune cell correlation analysis with pyroptosis-related hub genes. A regulatory network between pyroptosis-related hub genes and miRNA was also constructed, and protein domains were predicted. The expression of key pyroptosis genes was validated using an MCAO rat model. Twenty-five pyroptosis genes showed differential expression, including four hub genes, namely WISP2, MELK, SDF2L1, and AURKB. Characteristic genes were verified using real-time quantitative PCR analyses. The high- and low-risk groups showed significant expression differences for WISP2, MELK, and SDF2L1. In immune infiltration analysis, 12 immune cells showed differences in expression in MCAO samples. Further analysis demonstrated significant positive correlations between the pyroptosis-related hub gene SDF2L1 and immune cell-activated dendritic cells in the high-risk group and immune cell natural killer cells in the low-risk group. This study identified four pyroptosis-related hub genes, with elevated WISP2, MELK, and SDF2L1 expression closely associated with the high-risk group. The analysis of inflammatory cell types in immune infiltration can predict ischemic stroke risk levels and help to facilitate treatment.

摘要

中风是全球第二大致死原因。中风后缺血再灌注损伤（IRI）引发的免疫风暴造成的损害相当大。然而，关于IRI中细胞焦亡的转录组动力学数据有限。本研究旨在分析中风中关键细胞焦亡基因的表达及其与免疫浸润的相关性。从获得的大脑中动脉闭塞（MCAO）数据集中鉴定出细胞焦亡相关基因。对细胞焦亡相关基因进行差异表达和功能分析，并确定高风险组和低风险组之间功能富集的差异。使用选定的具有差异表达的细胞焦亡相关基因构建并验证MCAO诊断模型。构建高风险和低风险MCAO组，用于与细胞焦亡相关枢纽基因进行表达和免疫细胞相关性分析。还构建了细胞焦亡相关枢纽基因与miRNA之间的调控网络，并预测了蛋白质结构域。使用MCAO大鼠模型验证关键细胞焦亡基因的表达。25个细胞焦亡基因表现出差异表达，包括4个枢纽基因，即WISP2、MELK、SDF2L1和AURKB。使用实时定量PCR分析验证特征基因。高风险组和低风险组在WISP2、MELK和SDF2L1的表达上存在显著差异。在免疫浸润分析中，12种免疫细胞在MCAO样本中的表达存在差异。进一步分析表明，细胞焦亡相关枢纽基因SDF2L1与高风险组中的免疫细胞活化树突状细胞以及低风险组中的免疫细胞自然杀伤细胞之间存在显著正相关。本研究鉴定出4个细胞焦亡相关枢纽基因，WISP2、MELK和SDF2L1表达升高与高风险组密切相关。免疫浸润中炎症细胞类型的分析可以预测缺血性中风风险水平并有助于促进治疗。

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本文引用的文献

1
An analysis of AURKB's prognostic and immunological roles across various cancers.跨多种癌症的 AURKB 预后和免疫作用分析。
J Cell Mol Med. 2024 Jun;28(12):e18475. doi: 10.1111/jcmm.18475.
2
Dendritic cells as orchestrators of anticancer immunity and immunotherapy.树突状细胞作为抗癌免疫和免疫治疗的协调者。
Nat Rev Clin Oncol. 2024 Apr;21(4):257-277. doi: 10.1038/s41571-024-00859-1. Epub 2024 Feb 7.
3
Safety, tolerability, and pharmacokinetics of Aurora kinase B inhibitor AZD2811: a phase 1 dose-finding study in patients with advanced solid tumours.
Aurora 激酶 B 抑制剂 AZD2811 的安全性、耐受性和药代动力学：在晚期实体瘤患者中进行的 1 期剂量探索研究。
Br J Cancer. 2023 May;128(10):1906-1915. doi: 10.1038/s41416-023-02185-2. Epub 2023 Mar 4.
4
Pyroptosis: A Newly Discovered Therapeutic Target for Ischemia-Reperfusion Injury.细胞焦亡：缺血再灌注损伤的一个新的治疗靶点。
Biomolecules. 2022 Nov 3;12(11):1625. doi: 10.3390/biom12111625.
5
WISP-2 modulates the induction of inflammatory mediators and cartilage catabolism in chondrocytes.WISP-2 调节软骨细胞中炎症介质的诱导和软骨分解代谢。
Lab Invest. 2022 Sep;102(9):989-999. doi: 10.1038/s41374-022-00793-9. Epub 2022 Apr 28.
6
Childhood stroke.儿童中风。
Nat Rev Dis Primers. 2022 Feb 24;8(1):12. doi: 10.1038/s41572-022-00337-x.
7
World Stroke Organization (WSO): Global Stroke Fact Sheet 2022.世界卒中组织（WSO）：全球卒中状况 2022 概要。
Int J Stroke. 2022 Jan;17(1):18-29. doi: 10.1177/17474930211065917.
8
Inhibition of Aurora Kinase B activity disrupts development and differentiation of salivary glands.抑制极光激酶B的活性会破坏唾液腺的发育和分化。
Cell Death Discov. 2021 Jan 18;7(1):16. doi: 10.1038/s41420-020-00393-w.
9
CHRFAM7A Overexpression Attenuates Cerebral Ischemia-Reperfusion Injury via Inhibiting Microglia Pyroptosis Mediated by the NLRP3/Caspase-1 pathway.CHRFAM7A 通过抑制 NLRP3/Caspase-1 通路介导的小胶质细胞焦亡减轻脑缺血再灌注损伤。
Inflammation. 2021 Jun;44(3):1023-1034. doi: 10.1007/s10753-020-01398-4. Epub 2021 Jan 6.
10
Identification and Verification of Immune-Related Gene Prognostic Signature Based on ssGSEA for Osteosarcoma.基于单样本基因集富集分析（ssGSEA）的骨肉瘤免疫相关基因预后特征的鉴定与验证
Front Oncol. 2020 Dec 15;10:607622. doi: 10.3389/fonc.2020.607622. eCollection 2020.