Journal: Scientific Reports
Article Title: Finerenone ameliorates diabetic kidney disease exacerbated by deletion of natriuretic peptide/guanylyl cyclase-A signaling and dietary high-protein load
doi: 10.1038/s41598-025-25362-0
Figure Lengend Snippet: Podocyte damage and inflammatory changes are worsened by HPD in systemic GC-A knockout mice. ( a ) Immunohistochemical (IHC) staining for WT-1 in glomerulus. The graph shows the number of WT-1-positive cells per glomerulus as quantitative analysis. ( b ) IF staining for nephrin in each group. Scale Bar represents 50 μm. ( c ) Representative images of electron microscopic analysis in each group. The graphs indicate quantitative analysis of foot process width and GBM thickness. Scale Bar represents 1 μm. ( d ) IHC staining of MAC2 in glomerulus (▶). The graph shows the number of MAC2-positive macrophages per glomerulus. Scale Bar represents 50 μm. ( e , f ) Glomerular mRNA expression levels of Tgfb1 , Ctgf , Serpine1 , Ccl2 , Emr1 , Icam1 , and Vcam1 in each group. ( g ) Renal mRNA expression levels of Agt , Ren1 , and Sgk1 in each group. β-Actin ( Actb ) was used as internal control. Values are expressed as means ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, NS; not significant.
Article Snippet: Primary antibodies used for immunohistochemical and immunofluorescence studies were anti-GC-A antibody (GTX109810, GeneTex, Inc., Irvine, CA, USA), anti-MAC2 antibody (CL8942F, Cedarlane, Ontario, Canada), anti-Wilms tumor 1 (WT1) antibody (sc-15421, Santa Cruz Biotechnology, Dallas, TX), anti-nephrin antibody (AF3159, R&D Systems, Inc., Minneapolis, MN, USA), and anti-Tie2 antibody (AF762, R&D Systems, Inc.).
Techniques: Knock-Out, Immunohistochemical staining, Immunohistochemistry, Staining, Expressing, Control