Purpose: To clarify retinal control on scleral growth in form-deprivation myopia (FDM) in the chick, the authors studied change in transforming growth factor-beta (TGF-beta) in the form-deprived eye and the effect of this growth factor on scleral cell proliferation and axial length.
Methods: Change in TGF-beta in FDM in the chick was measured by reverse transcriptase polymerase chain reaction (RT-PCR), immunoblot, and immunohistochemistry. The effect of TGF-beta on [3H]thymidine uptake of scleral chondrocytes was determined by organ culture. Urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) were administered to determine the effect of TGF-beta activation on the axial length in normal and FDM eyes.
Results: The content of TGF-beta messenger RNA (mRNA) and the active form of TGF-beta protein were reduced in FDM eyes compared with the control specimen. Reduced immunoreactivity of TGF-beta in FDM eyes was found in the photoreceptor layer. The TGF-beta inhibited [3H]thymidine uptake into scleral chondrocytes. In the nondeprived eyes, the vitreous chamber depth and axial length were reduced after uPA treatment, whereas PAI-1 increased them. In the form-deprived eyes, uPA inhibited vitreous depth and axial length elongation, but PAI-1 had no effect.
Conclusions: The authors' results suggest that TGF-beta mediates retinal control of ocular growth. Axial elongation in FDM probably is correlated with the reduction of TGF-beta in the retina, retinal pigment epithelium, and choroid. The uPA and PAI-1 treatment controls the activation of TGF-beta and affects axial length.