RPCK1
Rao et al.
(2001) investigated the role of Rho kinase in the modulation of aqueous
humor outflow facility. The treatment of human trabecular meshwork and canal of
Schlemm cells with a Rho kinase-specific inhibitor led to significant but
reversible changes in cell shape and decreased actin stress fibers, focal
adhesions, and protein phosphotyrosine staining. Based on the Rho kinase
inhibitor-induced changes in myosin light chain phosphorylation and actomyosin
organization, the authors suggested that cellular relaxation and loss of cell-substratum
adhesions in the human trabecular meshwork and canal of Schlemm cells could
result in either increased paracellular fluid flow across the canal of Schlemm
or altered flow pathway through the juxtacanalicular tissue, thereby lowering
resistance to outflow. They suggested Rho kinase as a potential target for the
development of drugs to modulate intraocular pressure in glaucoma patients. 