Coding and long non-coding gene expression changes in the CNS traumatic injuries

Traumatic brain injury (TBI) and spinal cord injury (SCI) are two main central nervous system (CNS) traumas, caused by external physical insults. Both injuries have devastating effects on the quality of life, and there is no effective therapy at present. Notably, gene expression profiling using bulk...

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Bibliographic Details
Published inCellular and molecular life sciences : CMLS Vol. 79; no. 2; p. 123
Main Authors Wu, Xizi, Wei, Haichao, Wu, Jia Qian
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.02.2022
Springer Nature B.V
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Summary:Traumatic brain injury (TBI) and spinal cord injury (SCI) are two main central nervous system (CNS) traumas, caused by external physical insults. Both injuries have devastating effects on the quality of life, and there is no effective therapy at present. Notably, gene expression profiling using bulk RNA sequencing (RNA-Seq) and single-cell RNA-Seq (scRNA-Seq) have revealed significant changes in many coding and non-coding genes, as well as important pathways in SCI and TBI. Particularly, recent studies have revealed that long non-coding RNAs (lncRNAs) with lengths greater than 200 nucleotides and without protein-coding potential have tissue- and cell type-specific expression pattern and play critical roles in CNS injury by gain- and loss-of-function approaches. LncRNAs have been shown to regulate protein-coding genes or microRNAs (miRNAs) directly or indirectly, participating in processes including inflammation, glial activation, cell apoptosis, and vasculature events. Therefore, lncRNAs could serve as potential targets for the diagnosis, treatment, and prognosis of SCI and TBI. In this review, we highlight the recent progress in transcriptome studies of SCI and TBI and insights into molecular mechanisms.
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Authors’ contributions
XW, HW, and JQW wrote the manuscript. All authors read and approved the final manuscript.
ISSN:1420-682X
1420-9071
DOI:10.1007/s00018-021-04092-2