Some of the
cytokines and
growth factors in the aqueous humor activate Rho, and the Rho/ROCK signal transduction participates in signaling pathways via rearrangement of actin cytoskeleton that leads to various cellular reactions. In a previous study, we demonstrated that a selective ROCK inhibitor significantly reduced intraocular pressure, the mechanism of which was attributed to improved outflow. ROCK inhibitors induced the
actomyosin assembly, cell adhesive interactions, and the expression of extracellular matrix (ECM)
proteins in cultured TM cells. The inhibition of Rho also has been implicated in pathological wound healing by regulating neovascularization, migration, and ECM in
scar tissue. In this study, we investigated the role of ROCK inhibitor in regulating human Tenon fibroblast (HTF) activity and postoperative
scar formation in a rabbit
sclerostomy model. ROCK inhibitor showed decreased
aSMA expression in HTF, and prevented enhanced contractility, assembly of actin stress fibers, and myofibroblastic transdifferentiation. In vivo
sclerostomy studies showed that the
bleb survival was significantly improved in ROCK inhibitor-treated eyes. In another study by us, ROCK inhibitor showed
neuroprotective effects against rat
retinal ischemia reperfusion injury. Collectively, ROCK inhibitors are thus a potential new strategy for developing medical
therapy for glaucomatous dis-