Identification of primary genes in glomeruli compartment of immunoglobulin A nephropathy by bioinformatic analysis

Abstract

The current study is aimed to explore the specific genes which are responsible for the manifestation of Immunoglobulin A nephropathy (IgAN). Gene expression profiles GSE37460, GSE93798 and GSE104948 were analyzed using biological informatics methods to identify differentially expressed genes (DEGs) in IgAN glomeruli samples which were then compared to normal control samples. Subsequently, the DEGs were overlapped to explore genes with significant expression in at least two profiles. Finally, the enrichment analysis was conducted and the protein-protein interaction (PPI) network was constructed for the overlapping DEGs. A total of 28 genes were up-regulated and 10 genes were down-regulated. The up-regulated genes including CD44 and FN1 were chiefly involved in extracellular matrix receptors interaction pathway. In addition, CX3CR1 and CCL4 were associated with chemokine signaling pathway. ITGB2, PTPRC, FN1, and FCER1G were hub genes with a high degree of interaction in the PPI network. Therefore, this study identified many significant genes associated with extracellular matrix expansion and inflammatory mechanism which may be the novel biomarker and target candidates in IgAN.

Comprehensive analysis of IgA nephropathy expression profiles: identification of potential biomarkers and therapeutic agents

“…Re-analyzing and integration of omics-based expression profiles could be an advantageous tactic to catch a holistic view of the involving genes and miRNAs in the IgAN pathogenesis. Until now, several re-analyzes have been performed on the IgAN related expression profiles, mostly on kidney tissue samples of the patients [25][26][27][28].…”

Transmembrane signaling molecules play a key role in the pathogenesis of IgA nephropathy: a weighted gene co-expression network analysis study

“…For instance, in one experiment after reanalysis of two IgAN datasets, including GSE73953 and GSE93798, tumor nephrotic factor ( TNF ) and mitogen-activated protein kinase ( MAPK ) pathways were introduced as the key involved pathways in the IgAN pathogenesis [ 13 ]. Similarly, in another experiment, after analysis of three datasets, including GSE37460, GSE93798 and GSE104948, Miraji et al, revealed the association of “extracellular matrix receptors interaction pathways”, “extracellular matrix expansion” and “inflammatory mechanisms” with the pathogenesis of IgAN [ 14 ]. By construction of a PPI network among the overlapped DEGs and considering the degree of connectivity between the genes, the authors introduced several hub genes with therapeutic potentials including FN1 , ITGB2 , FCER1G and PTPRC [ 14 ].…”

“…Similarly, in another experiment, after analysis of three datasets, including GSE37460, GSE93798 and GSE104948, Miraji et al, revealed the association of “extracellular matrix receptors interaction pathways”, “extracellular matrix expansion” and “inflammatory mechanisms” with the pathogenesis of IgAN [ 14 ]. By construction of a PPI network among the overlapped DEGs and considering the degree of connectivity between the genes, the authors introduced several hub genes with therapeutic potentials including FN1 , ITGB2 , FCER1G and PTPRC [ 14 ].…”

Transmembrane Signaling Molecules Play a Key Role in Progression of IgA Nephropathy: A Weighted Gene Co-expression Network Analysis Study

“…For instance, in one experiment after reanalysis of two IgAN datasets, including GSE73953 and GSE93798, tumor nephrotic factor (TNF) and mitogen-activated protein kinase (MAPK) pathways were introduced as the key involved pathways in the IgAN progression (13). Similarly, in another experiment, after analysis of three datasets, including GSE37460, GSE93798 and GSE104948, Miraji et al, revealed the association of "extracellular matrix receptors interaction pathways", "extracellular matrix expansion" and "in ammatory mechanisms" with the progression of IgAN (14). By construction of a PPI network among the overlapped DEGs and considering the degree of connectivity between the genes, the authors introduced several hub genes with therapeutic potentials including FN1, ITGB2, FCER1G and PTPRC (14).…”