Gene Expression Signature of Traumatic Brain Injury

Ma, Yuhang; Liu, Yunhui; Ruan, Xuelei; Liu, Xiaobai; Zheng, Jian; Teng, Hao Wei; Shao, Lianqi; Yang, Chunqing; Wang, Di; Xue, Yixue

doi:10.3389/fgene.2021.646436

Cited by 11 publications

(8 citation statements)

References 43 publications

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“…Some novel biomarkers for NOA were also screened. Ribosomal Protein S4 X-Linked (RPS4X) was essential for the formation of cytoplasmic ribosomes and participated in the initiation and progression of multiple diseases [ 29 – 31 ]. RPS4X acted as the strongest predictor in the random forest model with the highest Mean Decrease Accuracy and Mean Decrease Gini.…”

Section: Discussionmentioning

confidence: 99%

Construction and external validation of a 5-gene random forest model to diagnose non-obstructive azoospermia based on the single-cell RNA sequencing of testicular tissue

Zhou

Chen

et al. 2021

Aging

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Section: Discussionmentioning

confidence: 99%

Construction and external validation of a 5-gene random forest model to diagnose non-obstructive azoospermia based on the single-cell RNA sequencing of testicular tissue

Zhou

Chen

et al. 2021

Aging

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“…Genetic analysis can elucidate the genetic influence on post-TBI outcomes and would allow precision treatment based on genetic traits. In analysis of a large biologic database, genetic modules that showed greatest change in expression were primarily associated with neurodevelopment and immune inflammation [133]. As previously discussed, the ApoE-4 allele is also of special interest in the field of chronic TBI-induced inflammation.…”

Section: Omics-based Biomarkersmentioning

confidence: 93%

“…ApoE protein is a mediator of cholesterol and lipid transport in the brain and has been shown to attenuate glial activation and CNS inflammatory responses. In experimental models, a small peptide of ApoE [133][134][135][136][137][138][139][140][141][142][143][144][145][146][147][148][149] was shown to significantly improve histological and functional outcomes following TBI [134].…”

Section: Omics-based Biomarkersmentioning

confidence: 99%

Neuroinflammation in Traumatic Brain Injury

Kuo¹,

Tarzi²,

Louie³

et al. 2022

Frontiers in Traumatic Brain Injury

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Neuroinflammation following traumatic brain injury (TBI) is an important cause of secondary brain injury that perpetuates the duration and scope of disease after initial impact. This chapter discusses the pathophysiology of acute and chronic neuroinflammation, providing insight into factors that influence the acute clinical course and later functional outcomes. Secondary injury due to neuroinflammation is described by mechanisms of action such as ischemia, neuroexcitotoxicity, oxidative stress, and glymphatic and lymphatic dysfunction. Neurodegenerative sequelae of inflammation, including chronic traumatic encephalopathy, which are important to understand for clinical practice, are detailed by disease type. Prominent research topics of TBI animal models and biomarkers of traumatic neuroinflammation are outlined to provide insight into the advances in TBI research. We then discuss current clinical treatments in TBI and their implications in preventing inflammation. To complete the chapter, recent research models, novel biomarkers, and future research directions aimed at mitigating TBI will be described and will highlight novel therapeutic targets. Understanding the pathophysiology and contributors of neuroinflammation after TBI will aid in future development of prophylaxis strategies, as well as more tailored management and treatment algorithms. This topic chapter is important to both clinicians and basic and translational scientists, with the goal of improving patient outcomes in this common disease.

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“…We used the key word “traumatic brain injury” and “epilepsy” to search TBI and epilepsy gene expression data from the Gene Expression Omnibus (GEO) 1 and published researches. Two microarray datasets GSE104687 ( Miller et al, 2017 ; Ma et al, 2021 ) and GSE143272 ( Rawat et al, 2020 ) were downloaded, and were regarded as the discovery cohort. The GSE104687 dataset contains 93 TBI samples and 103 samples without TBI, and GSE143272 consists of 34 samples with epilepsy and 50 healthy samples as the control group.…”

Section: Methodsmentioning

confidence: 99%

Exploring the pathogenesis linking traumatic brain injury and epilepsy via bioinformatic analyses

Zhao

Fu²,

Yang³

et al. 2022

Front. Aging Neurosci.

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Traumatic brain injury (TBI) is a serious disease that could increase the risk of epilepsy. The purpose of this article is to explore the common molecular mechanism in TBI and epilepsy with the aim of providing a theoretical basis for the prevention and treatment of post-traumatic epilepsy (PTE). Two datasets of TBI and epilepsy in the Gene Expression Omnibus (GEO) database were downloaded. Functional enrichment analysis, protein–protein interaction (PPI) network construction, and hub gene identification were performed based on the cross-talk genes of aforementioned two diseases. Another dataset was used to validate these hub genes. Moreover, the abundance of infiltrating immune cells was evaluated through Immune Cell Abundance Identifier (ImmuCellAI). The common microRNAs (miRNAs) between TBI and epilepsy were acquired via the Human microRNA Disease Database (HMDD). The overlapped genes in cross-talk genes and target genes predicted through the TargetScan were obtained to construct the common miRNAs–mRNAs network. A total of 106 cross-talk genes were screened out, including 37 upregulated and 69 downregulated genes. Through the enrichment analyses, we showed that the terms about cytokine and immunity were enriched many times, particularly interferon gamma signaling pathway. Four critical hub genes were screened out for co-expression analysis. The miRNA–mRNA network revealed that three miRNAs may affect the shared interferon-induced genes, which might have essential roles in PTE. Our study showed the potential role of interferon gamma signaling pathway in pathogenesis of PTE, which may provide a promising target for future therapeutic interventions.

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Gene Expression Signature of Traumatic Brain Injury

Cited by 11 publications

References 43 publications

Construction and external validation of a 5-gene random forest model to diagnose non-obstructive azoospermia based on the single-cell RNA sequencing of testicular tissue

Construction and external validation of a 5-gene random forest model to diagnose non-obstructive azoospermia based on the single-cell RNA sequencing of testicular tissue

Neuroinflammation in Traumatic Brain Injury

Exploring the pathogenesis linking traumatic brain injury and epilepsy via bioinformatic analyses

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