(A) Podocytes treated with NTS show damaged actin cytoskeleton (Green) with accumulation of actin stress fibers at cell periphery, and loss of Neph1 (Red) at the cell-cell junctions. In contrast, significant recovery of actin cytoskeletal organization was noted in formoterol treated cells along with restoration of Neph1 staining at cell-cell junctions (arrows). Scale bar 20μm. (B) The quantitative analysis showed ~27% increase in the number of healthy podocytes with a concomitant decrease in NTS injured podocytes upon formoterol treatment, while the vehicle treated podocytes recovered minimally. (C) Quantitation further showed complete relocalization of Neph1 at cell membrane upon formoterol treatment of NTS injured podocytes. Data are presented in mean±SEM, One-way ANOVA, ###P≤0.0001 vs. untreated control; ***P≤0.0001 NTS+vehicle vs. NTS+formoterol. (D) PS injured podocytes showed damaged actin cytoskeleton (Green) with accumulation of actin stress fibers at cell periphery, and loss of Neph1 (Red) at the cell-cell junctions. Recovery of actin cytoskeletal organization was noted in formoterol treated cells with restoration of Neph1 staining at the cell junctions (arrows). Scale bar 20μm. (E) The quantitative analysis of actin cytoskeleton reorganization showed significant increase in the number of healthy podocytes (~40%), with a concomitant decrease in PS injured podocytes upon treatment with formoterol, whereas the recovery in vehicle treated podocytes was minimal. (F) The quantitative assessment of Neph1 relocalization at podocyte cell membrane shows, complete relocalization of Neph1 at cell membrane in formoterol treated PS injured podocytes. Data are presented in mean±SEM, One-way ANOVA, ###P≤0.0001 vs. untreated control; *** P≤0.0001 PS+vehicle vs. PS+formoterol.