Table 1.
Primers used in current study.
Fig 1.
Functional enrichment analysis of differentially expressed genes (DEGs) in lupus nephritis.
A Volcano plot of DEGs in LN and normal control samples. Blue dots represent significantly downregulated DEGs in the samples, and red dots represent significantly upregulated DEGs. B GO functional enrichment analysis was performed on the upregulated DEGs, and the top 10 of biological process (BP), cell component (CC), and molecular function (MF) terms were selected to draw a bar graph. C Functional enrichment of upregulated DEGs analyzed by DAVID, with the top 15 pathways shown by bubble plot. D 13 DEGs enriched in the NOD-like receptor signaling pathway were imported into the STRING database, and the protein interaction network was processed with Cytoscape. E The top 5 hub DEGs were obtained by using the MCC algorithm of the Cytohubba plug-in in Cytoscape software.
Table 2.
Age and gender distribution in the lupus nephritis and control groups.
Fig 2.
Immunohistochemical analysis of GBP2 and GSDMD in pediatric lupus nephritis.
A Representative immunohistochemical images (400 × magnification; scale bar, 50 μm) of renal sections from pediatric Lupus nephritis (LN) and control renal tissues, showing the expression and localization of GBP2 and GSDMD in glomeruli and tubules. B Glomerular areas were manually outlined in five randomly selected 400 × fields for mean optical density quantification. Correlation analyses of glomerular GBP2 or GSDMD expression with proteinuria in pediatric LN patients (n = 50) were shown, with statistical significance determined by Spearman correlation.
Fig 3.
Characterization of renal injury, GBP2 expression, and pyroptosis in LN mice.
A Evaluation of urinary protein-creatinine ratio, kidney-to-body weight ratio, blood urea nitrogen and anti-dsDNA antibody levels in control and Lupus nephritis (LN) mice. B Representative immunohistochemical staining of renal tissues in control and LN mice (400 × magnification; scale bar, 50 μm). C Evaluation of pyroptosis-related mRNA levels by RT-qPCR. D Evaluation of pyroptosis-related protein levels by western blotting. Data were expressed as the mean ± SD (n = 6 per group). *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 4.
Effects of Gbp2 silencing on pyroptosis and inflammation in MPC-5 cells.
A Evaluation of siRNA knockdown efficiency by RT-qPCR and western blotting. B Evaluation of pyroptosis-related mRNA levels by RT-qPCR. C Evaluation of pyroptosis-related protein levels by western blotting. D Evaluation of inflammatory cytokines by ELISA. Data were expressed as the mean ± SD (n = 3 independent biological replicates). *P < 0.05, **P < 0.01, ***P < 0.001; ns, not significant.
Fig 5.
Effects of Gbp2 overexpression on LPS/ATP-induced pyroptosis and inflammation in MPC-5 cells.
A Evaluation of plasmid overexpression efficiency by RT-qPCR and western blotting. B Evaluation of pyroptosis-related mRNA levels by RT-qPCR. C Evaluation of pyroptosis-related protein levels by western blotting. D Evaluation of inflammatory cytokines by ELISA. Data were expressed as the mean ± SD (n = 3 independent biological replicates). *P < 0.05, **P < 0.01, ***P < 0.001; ns, not significant.
Fig 6.
Aim2 overexpression rescues the inhibitory effects of Gbp2 knockdown on pyroptosis in MPC-5 cells.
A Evaluation of plasmid overexpression efficiency by western blotting. B Evaluation of pyroptosis-related mRNA levels by RT-qPCR. C Evaluation of pyroptosis-related protein levels by western blotting. D Cell viability (assessed by CCK-8 assay) and plasma membrane damage (assessed by LDH release assay) across treatment groups. E Evaluation of inflammatory cytokines by ELISA. Data were expressed as the mean ± SD (n = 3 independent biological replicates). *P < 0.05, **P < 0.01, ***P < 0.001; ns, not significant.