Receptor Activator of NF-kappaB and Podocytes: Towards a Function of a Novel Receptor-Ligand Pair in the Survival Response of Podocyte Injury
Figure 2
Expression of RANK and RANKL in Human Podocyte Injury Diseases.
(A) RANK protein (red) was expressed in glomeruli of human kidney. RANK was found in podocytes, as shown by double immunofluorescence with the podocyte marker synaptopodin (green) resulting in yellow overlap (Merge). Compared with control, immunofluorescence staining for RANK was increased in IgA nephropathy, MN and FSGS, double immunofluorescence staining revealed that the increase in RANK protein expression was mainly attributed to podocytes. There was no immunfluoresence in the glomerulosclerosis position of FSGS. (B) RANK mRNA was expressed in human kidneys. Quantitative real-time RT-PCR was performed on kidney tissue from human biopsies. RANK mRNA was low in individuals without glomerular disease. By contrast, individuals with biopsy-proven FSGS, IgA nephropathy and MN had a significant increase in RANK expression (FSGS 0.42±0.07, IgA nephropathy 0.37±0.10, MN 0.67±0.24, versus control 0.24±0.04). *Compared with control, p<0.01. (C) Quantitative real-time RT-PCR was performed on kidney tissue from human biopsies. RANKL mRNA was low in individuals without glomerular disease. By contrast, individuals with FSGS, IgA nephropathy and MN had a moderate increase in RANKL expression (FSGS 0.25±0.07, IgA nephropathy 0.22±0.08, MN 0.27±0.08, versus control 0.11±0.05). *Compared with control, p<0.01.