Data for the manuscript entitled: A novel role of neutrophil elastase in podocyte dysfunction induced by high glucose, PMA, and MDP.

Data for the manuscript entitled: A novel role of neutrophil elastase in podocyte dysfunction induced by high glucose, PMA, and MDP.This dataset accompanies a study investigating the immunological properties of podocytes and their capacity to produce and secrete neutrophil serine proteases (NSPs). We demonstrate that podocytes synthesize neutrophil elastase (NE), proteinase 3 (PR3), and cathepsin G (CatG), and release their active forms into the extracellular space. Using models of inflammation (PMA stimulation) and insulin insensitivity, we show that NSP activity contributes to podocyte dysfunction. Activation of the NOD2 receptor by muramyl dipeptide (MDP) induced actin cytoskeleton rearrangement and increased albumin permeability, accompanied by elevated NE and PR3 activity. Silencing the ELANE gene, encoding NE, attenuated these pathological responses. The data provided here support the conclusion that NSPs—particularly NE—play a pathogenic role in podocyte injury associated with inflammation, insulin resistance, and diabetic kidney disease.These data were used to create Figures 1-6. All data for Figures have been included in the file Figure 1–6.