ROCK as a Therapeutic Target of Diabetic Retinopathy

Figure 1

Rho/ROCK activation in retinal vessels. In immunohistochemical analysis, RhoA (a), ROCK1 (b) and ROCK2 (c) were detected in retinal vessels. Yellow (white arrowhead) indicates double-stained vasculature (magnification: $\times 400$). (d and e) The levels of Rho-GTP were significantly higher in streptozotocin induced-diabetic rat bretinas, compared with those in nondiabetic control, detected by Rho pull-down assay. Average signal intensities are quantified and expressed as percentage of the ratio of control (${}^{**}P<.01,\hspace{0.17em}\hspace{0.17em}n=5$ each). Prevention of leukocyte-induced retinal endothelial damage by fasudil. (f–i) In vivo visualization of adhering leukocytes (green, concanavalin A lectin) and injured endothelial cells (red, propidium iodide (PI)) and endothelial nuclei (blue, DAPI) in rat retinas. PI positive cells (white arrowhead) widely coincided with adherent leukocytes (white arrow). The number of PI positive cells per retina was significantly higher in the diabetic animals, compared with the nondiabetic controls. Fasudil caused a significant reduction in the number of PI positive cells in the retinas of the diabetic animals, compared with the vehicle-treated controls (${}^{**}P<.01$, N.S., not significant, $n=5$ each).