PLASMINOGEN-ACTIVATOR (UROKINASE) CAUSES VASCULARIZATION OF THE CORNEA

  • 1 January 1982
    • journal article
    • research article
    • Vol. 22  (2) , 191-199
Abstract
The presence of a peripheral zone of (presumed intracellular) plasminogen activator in the normal rabbit cornea suggested that activator, once released, might regulate the permeability of limbal vessels and angiogenesis, by plasmin-dependent pathways. Plasminogen activator (urokinase [UK]) in rabbit serum albumin (RSA) was injected once (20 .mu.l, 3.7 CTA U [committee on thrombolytic agents units]) into the corneal stroma, 2 mm from the limbus. Sprouting from the engorged circumlimbal vessels (16 of 20 corneas) began on the 3rd day and grew into the cornea over the next several days. Histologically, PMN [polymorphonuclear leukocyte] were observed in association with growing vessels. Contralateral corneas injected with UK (in RSA) previously inactivated by 99.7% with the specific active site inhibitor, Phe-Ala-Arg-chloromethyl ketone showed minimal vessel engorgement or stromal edema and no vascularization (0-20 corneas). Injuries to the so-called (plasminogen activator-containing) critical zone of the cornea which elicit neovascularization possibly do so by causing extracellular release of endogenous plasminogen activator. In addition to initiating the destructive events of ulceration, activator might initiate increases in vessel permeability and also neovascularization, which would result in the eventual arrest of ulceration.