ArticleMolecular medicine reports2019
Identification of critical genes associated with spinal cord injury based on the gene expression profile of spinal cord tissues from trkB.T1 knockout mice.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- TrkB Truncated Isoform Receptors as Transducers and Determinants of BDNF Functions.Frontiers in neuroscience · 2022Pooled it
- Interplay of axon regeneration genes and immune infiltration in spinal cord injury.Journal of translational medicine · 2025Article
- Revealing Potential Spinal Cord Injury Biomarkers and Immune Cell Infiltration Characteristics in Mice.Frontiers in genetics · 2022Article
- Systemic gene expression profiles according to pain types in individuals with chronic spinal cord injury.Molecular painArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to identify the genes and underlying mechanisms critical to the pathology of spinal cord injury (SCI). Gene expression profiles of spinal cord tissues of trkB.T1 knockout (KO) mice following SCI were accessible from the Gene Expression Omnibus database. Compared with trkB.T1 wild type (WT) mice, the differentially expressed genes (DEGs) in trkB.T1 KO mice following injury at different time points were screened out. The significant DEGs were subjected to function, co‑expression and protein‑protein interaction (PPI) network analyses. A total of 664 DEGs in the sham group and SCI groups at days 1, 3, and 7 following injury were identified. Construction of a Venn diagram revealed the overlap of several DEGs in trkB.T1 KO mice under different conditions. In total, four modules (Magenta, Purple, Brown and Blue) in a co‑expression network were found to be significant. Protein tyrosine phosphatase, receptor type C (PTPRC), coagulation factor II, thrombin (F2), and plasminogen (PLG) were the most significant nodes in the PPI network. 'Fc γ R‑mediated phagocytosis' and 'complement and coagulation cascades' were the significant pathways enriched by genes in the PPI and co‑expression networks. The results of the present study identified PTPRC, F2 and PLG as potential targets for SCI treatment, which may further improve the general understanding of SCI pathology.
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