ArticleIbrain2022
The differentially expressed proteins related to clinical viral encephalitis revealed by proteomics.
Article in Ibrain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Integrated Analysis of Cortex Single-Cell Transcriptome and Serum Proteome Reveals the Novel Biomarkers in Alzheimer's Disease.Brain sciences · 2022Article
- Understanding global changes of the mouse brain proteome after vaginal infection with HSV-2 using a label-free shotgun approach.Frontiers in cellular and infection microbiology · 2022Article
- The differentially expressed proteins related to clinical viral encephalitis revealed by proteomics.Ibrain · 2022Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To screen out the prospective biomarkers of viral encephalitis (VE), analyze the biological process and signaling pathways involved by differentially expressed proteins (DEPs). A total of 11 cerebrospinal fluid (CSF) samples with VE and 5 with non-nervous system infection were used to perform label-free proteomic techniques. Then, the bioinformatic analysis of DEPs was applied by Interproscan software. Moreover, 73 CSF samples in the VE group and 53 in the control group were used to verify the changes of some DEPs by enzyme-linked immunosorbent assay (ELISA). Thirty-nine DEPs were identified, including 18 upregulated DEPs and 21 downregulated DEPs. DEPs were mainly enriched in cell adhesion molecules by Kyoto Encyclopedia of Genes and Genomes analysis pathway analysis. The DEPs related to axon tissue were obviously downregulated and the most significant downregulated proteins were neurexin 3, neurofascin, and neuroligin 2 (NLGN2). Moreover, the protein expression of NLGN2 in the VE group was significantly higher than that in the control group by ELISA. The correlation analysis of NLGN2 in the VE group revealed that there was a weak positive correlation with CSF protein and a weak negative correlation with CSF chloride. The clinical VE may be closely related to NLGN2 and the cell adhesion molecule pathway.
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