Plasminogen Activator: Influence on Axial Length in Chick Eye
Transforming growth factor β (TGF-β) is thought to be a regulator of the development of form-deprivation myopia (FDM) in the chick. We investigated the change in axial length when TGF-β was activated by plasminogen activator, which is a major biologic activator of TGF-β. White leghorn chicks were treated with or without lid suture of the right eye for 10 days. Daily retrobulbal injection of (1) urokinase-plasminogen activator (uPA), (2) plasminogen activator inhibitor-1 (PAI-1), a specific inhibitor of PA, or (3) saline was performed in the right eyes of lid-sutured and nonsutured chicks. The same volume of saline was injected in the left eyes of chicks for a control. At the end of each drug trial the anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured with ultrasonography. No significant change was detected in ACD or LT in the control and uPA-treated eyes or between the control and PAI-1-treated eyes with or without lid suture. In the eyes of non-lid-sutured chicks, the uPA inhibited VCD and AL, whereas PAI-1 enlarged them. In lid-sutured eyes, uPA inhibited VCD and AL, but PAI-1 showed no effect. These results suggest that activation of TGF-β influences the control of axial length in form-deprived and even nondeprived eyes.