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Urinary proteomics of Henoch-Schönlein purpura nephritis in children using liquid chromatography-tandem mass spectrometry

BACKGROUND: Henoch-Schönlein purpura nephritis (HSPN) is the principal cause of morbidity and mortality in children with Henoch-Schönlein purpura (HSP). However, the criteria for risk assessment currently used is not satisfactory. The urine proteome may provide important clues to indicate the develo...

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Detalles Bibliográficos
Autores principales: Fang, Xiang, Wu, Heyan, Lu, Mei, Cao, Yan, Wang, Ren, Wang, Meiqiu, Gao, Chunlin, Xia, Zhengkun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066733/
https://www.ncbi.nlm.nih.gov/pubmed/32190014
http://dx.doi.org/10.1186/s12014-020-09274-x
Descripción
Sumario:BACKGROUND: Henoch-Schönlein purpura nephritis (HSPN) is the principal cause of morbidity and mortality in children with Henoch-Schönlein purpura (HSP). However, the criteria for risk assessment currently used is not satisfactory. The urine proteome may provide important clues to indicate the development of HSPN. METHODS: Here, we detected and compared the urine proteome of patients with HSPN and healthy controls by liquid chromatography-tandem mass spectrometry (LC–MS/MS) in the data-independent acquisition (DIA) mode. The differentially expressed proteins were analysed by gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. For validation, enzyme-linked immunosorbent assay (ELISA) was used to analyse the selected proteins. RESULTS: A total of 125 proteins (29 upregulated and 96 downregulated) were found to be differentially expressed in children with HSPN compared with the controls. Forty-one proteins were predicted to have direct interactions. The enriched pathways mainly included focal adhesion, cell adhesion molecules, the PI3K-Akt signalling pathway, ECM-receptor interactions and so on. Cell adhesion related to the pathogenesis of HSPN was the main biological process identified in this study. The decrease in two proteins (integrin beta-1 and tenascin) was validated by ELISA. CONCLUSIONS: Our study provides new insights into the assessment of HSPN progression in children, as well as new potential biomarkers. The data confirm the value of the urinary proteome in capturing the emergence of HSPN.