Transcriptomic and proteomic landscape of Vogt-Koyanagi-Harada disease
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Yes
Purpose
To uncover the transcriptomic and proteomic landscape of Vogt-Koyanagi-Harada (VKH) disease and comprehensively understand the underlying pathogenesis mechanism.
Methods
RNA sequencing and Isobaric Tags for Relative and Absolute Quantitation based proteomics were used to measure mRNAs and proteins expression profiling of CD4+ T cells from patients with active VKH patients and healthy controls. Bioinformatic analysis was used to enrich the immune-inflammation related molecules. Quantitative real time PCR and Parallel Reaction Monitoring were used to validate candidate molecules that differentially expressed at both levels of mRNAs and proteins. Gain/loss-of-function experiments in vitro were performed to validate potential mediators.
Results
We found that the PARP10 expression was increased in CD4+ T cells of active VKH patients compared to that of healthy controls, and its expression was controlled by YBX1 transcriptionally. Also, we found that downstream molecules regulated by PARP10 were enriched in autophagy pathways.
Conclusion
This study is attended to reveal a new signaling axis dominated by YBX1/PARP10 to regulate the pathogenesis of VKH disease, which could provide potential targets for the diagnosis and therapy of the disease.
Conflict of interest
No
1
Last name
CHANG
Initials of first name(s)
Rui
Department
the first affiliated hospital of Chongqing medical university
City
Chongqing
Country
China
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