Microarray for whole mouse genome (Exon Array) for FFSS

To study the gene expression changes following application of Fluid Flow Shear Stress (FFSS) stimulus at end, post-2hr and post-24hr on mouse podocytes. We and others have started rethinking the concept of hyperfiltration as relative to changes in local biomechanical forces within the glomerulus. We believe that investigating the interplay of biomechanical forces on podocytes within the glomerulus may provide a better understanding of hyperfiltration-mediated kidney injury. The flow of glomerular ultrafiltrate creates shear stress on the surface of the podocyte. FFSS is largely exerted over the exposed outer aspect of major processes and the soma of podocytes. Our previous work suggests that COX2-PGE2-EP2 axis plays an important role in hyperfiltration-mediated injury, and targeting the EP2 receptor may have therapeutic significance. Thus to date we have identified COX-2-PGE2-EP2 axis in ‘mechanoperception’. The next logical step in this pursuit will be to address ‘mechanotransduction’, i.e. how podocyte converts the mechanical stimulus into biochemical signals that elicit specific cellular responses. To address this we took the approach of big data analysis using whole exon array analysis following application of FFSS to podocytes, and then selecting and validating pathways identified by bioinformatics tools that held biological relevance in FFSS in other epithelial cells and in EP2-mediated signaling. 12 samples were analyzed. The samples were performed in triplicated for Control sample, for end of FFSS (end), at 2 hours following completion of FFSS (post-2hr) and 24 hours following completion of FFSS (post-24hr)