Gene expression profile of Randall's Plaque tissue

Randall’s plaque (RP) is the origin of renal calcification on which idiopathic calcium oxalate (CaOx) kidney stones develop. To establish genomic pathogenesis of RP, we performed the microarray analysis for comparing the gene expressions among renal papillary RP and normal tissue of 23 CaOx and 6 calcium phosphate (CaP) stone formers, and normal papillary tissue of 7 control patients. Compare to normal papillary tissue, RP tissue contained up-regulation of lipocalin 2, interleukin 11, prostaglandin-endoperoxide synthase 1, glutathione peroxidase 3, and monocyte to macrophage differentiation, whereas down-regulation of solute carrier family 12 member 1 and sodium leak channel non selective (either > 2.0- or 0.5-fold, p <0.01). The network and toxicity analysis showed these genes had association with activated mitogen-activated protein kinase, Akt/ phosphatidylinositol 3-kinase pathway, and pro-inflammatory cytokines, which caused renal injury and oxidative stress. Human renal papillary tip tissues were biopsied during endoscopic kidney stone surgery. Tissues including Randall's Plaque from calcium stone former was designed as P group, normal papillary tissue from calcium stone former was designed as N group, and normal papillary tissue from control patients without any kidney stone was designed as C group. Comparison among P, N, and C group was performed.