ArticleJournal of inflammation research2025
Usp18 Mediates D-Dopachrome Tautomerase-Induced Astrocytic Inflammation After Spinal Cord Injury.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Role of the miR-340-5p/IRF1/USP18 Axis in Neuroinflammation Associated with Epilepsy.Neurochemical research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: D-dopachrome tautomerase (D-DT), a homolog of macrophage migration inhibitory factor (MIF), has been revealed to promote astrocytic inflammation and worsen neuropathology following spinal cord injury (SCI). So far, the mechanism about D-DT-activated astrocytic inflammation remains elusive. Ubiquitin-specific peptidase 18 (Usp18) is an active player in regulating innate immunity through ISG15-deconjugated dependent or independent manner in multiple cell types. Whether D-DT activates astrocytic inflammation Methods: SCI model was prepared by cord contusion at T8-T10 of rats. The expression changes of D-DT and Usp18 were examined by ELISA, Western blot, RT-PCR or immunohistochemistry. Primary astrocytes were treated by different concentration of D-DT, either for transcriptome sequencing or for analysis of D-DT-mediated expression of Usp18. Knockdown of CD74 or Usp18 expression was performed by siRNA transfection of astrocytes. The locomotor functions were assessed using the Basso, Beattie, and Bresnahan (BBB) locomotor scale. Results: Usp18 was significantly upregulated in the astrocytes at lesion sites following SCI, in parallel with the elevation of D-DT protein levels. D-DT inhibitor 4-CPPC remarkably decreased the astrocytic expression of USP18. Transcriptome sequencing of D-DT-stimulated primary astrocytes identified that Usp18 was the hub modulator of D-DT-mediated astrocytic inflammation. D-DT-mediated expression of Usp18 was able to activate MAPKs, contributing to the production of proinflammatory cytokines and chemokines. Specifically, phosphorylation of P38 kinase was shown to promote the expression of Usp18 by formation of a positive feedback loop. Administration of D-DT inhibitor 4-CPPC at lesion sites following SCI significantly reduced the protein levels of Usp18 and ameliorated functional deficits of rat hindlimb locomotion. Conclusion: SCI-induced elevation of D-DT at lesion sites activates astrocytic inflammation
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.