iTRAQ quantitative proteomic analysis differentially expressed proteins and signal pathways in henoch-schönlein purpura nephritis.

Henoch-Schönlein purpura nephritis (HSPN) has been considered as a major cause of chronic renal failure in children and a condition which can worsen clinical outcomes in adults. At present, the molecular mechanisms of HSPN are still unclear. In this study, iTRAQ quantitative proteomic analysis was performed on renal tissues collected from patients with HSPN and compared with those of patients after nephrectomy (controls). A total of 149 differentially expressed proteins (DEPs) were detected, of which, 97 being upregulated and 52 down-regulated. Protein functions and classifications were analyzed using Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). In addition, protein domains. expressive hierarchical clustering analysis and protein-protein interaction (PPI) analysis were also conducted for DEPs. The results of bioinformatics analysis indicated that DEPs were enriched in lipid metabolism and the adherens junction pathway. Among these proteins, CDC42 and CTNNB1 were identified as potential candidates involved in the pathogenesis of HSPN. Immunohistochemistry and real-time PCR further demonstrated that CDC42 and CTNNB1 were up-regulated in HSPN patients. These results provide new and important insights into some underlying molecular pathogenesis of HSPN.