Low-dose cadmium activates the JNK signaling pathway in human renal podocytes

Cadmium (Cd) is an environmental toxin. Our previous study demonstrated that low-dose Cd damages the integrity of the glomerular filtration barrier (GFB); however, the underlying mechanisms are poorly understood. Podocytes are a major component of the GFB, which regulate the passage of proteins. The present study aimed to investigate the effects of low-dose Cd on human renal podocytes (HRPs). HRPs were treated with Cd and activation of the c-Jun N-terminal kinase (JNK) pathway was examined by western blot analysis. Proliferation, viability and apoptosis of HRPs were evaluated by MTT assay, trypan blue exclusion assay and flow cytometry, respectively. The properties of HRPs were validated by immunofluorescence staining and Phalloidin-labeling. The results indicated that 4 M Cd may activate the JNK pathway, and increase the protein expression levels of c-Jun and c-Fos. However, proliferation, viability, apoptosis and alignment of the F-actin cytoskeleton in HRPs were not significantly affected by Cd treatment, with or without SP600125 pretreatment. In addition, the expression levels of CD2-associated protein and synaptopodin, which are differentiation markers of HRPs, remained unchanged following Cd treatment. These results indicated that low-dose Cd activates the JNK pathway but does not significantly affect HRP function.