Abstract
Background Although Henoch-Schönlein purpura nephritis (HSPN) is characterized by glomerular deposition of aberrantly glycosylated immunoglobulin A1 (IgA1), the underlying mechanism of HSPN progression has not yet been completely elucidated. In this study, we integrated transcriptomic and proteomic analyses to explore the underlying mechanism of HSPN progression. Methods RNA sequencing and tandem mass tag- (TMT-) based quantitative proteomics were used to gain serum transcriptomic and proteomic profiles of patients with different types of HSPN (3 × type 1, 3 × type 2, and 3 × type 3). Student's t-tests were performed to obtain the significance of the differential gene expression. The clusterProfiler package was used to conduct the functional annotation of the DEGs for both Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways. Results A total of 2315 mRNAs and 30 proteins were differentially expressed between the different types of HSPN. 58 mRNAs and one protein changed continuously during HSPN development and are potential biomarkers for HSPN progression. The validation cohort (another 9 patients) confirmed the high-throughput results of the transcriptomic and proteomic analyses. A total of 385 significant pathways were related to HSPN progression, and four of them were closely related to clinical biochemical indicators and may play an important role in the progression of HSPN. Those pathways reveal that HSPN progression may be related to the inhibition of inflammation, promotion of apoptosis, and repair of renal injury. Conclusions Four pathways were found to be closely related to HSPN progression, and it seems that HSPN progression is mainly due to the inhibition of inflammation, promotion of apoptosis, and repair of renal injury.
Highlights
Henoch-Schönlein purpura nephritis (HSPN) is the most serious complication of Henoch-Schönlein purpura (HSP) and occurs in approximately 30% of HSP pediatric patients within 4-6 weeks of the initial presentation [1,2,3]
It was found that a total of 2315 mRNAs and 30 proteins were differentially expressed between different types of HSPN (Supplementary Table S2 and Supplementary Table S3)
They mainly were found to be involved in immunity, apoptosis, platelet and coagulation, and tumor necrosis, consistent with the pathway enrichment results, and those functions were related to nephritis and renal injury [10, 15, 19]
Summary
Henoch-Schönlein purpura nephritis (HSPN) is the most serious complication of Henoch-Schönlein purpura (HSP) and occurs in approximately 30% of HSP pediatric patients within 4-6 weeks of the initial presentation [1,2,3]. Henoch-Schönlein purpura nephritis (HSPN) is characterized by glomerular deposition of aberrantly glycosylated immunoglobulin A1 (IgA1), the underlying mechanism of HSPN progression has not yet been completely elucidated. A total of 385 significant pathways were related to HSPN progression, and four of them were closely related to clinical biochemical indicators and may play an important role in the progression of HSPN. Those pathways reveal that HSPN progression may be related to the inhibition of inflammation, promotion of apoptosis, and repair of renal injury. Four pathways were found to be closely related to HSPN progression, and it seems that HSPN progression is mainly due to the inhibition of inflammation, promotion of apoptosis, and repair of renal injury
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