AIM: To explore the mechanism of Smad1 during form-deprivation myopia development in C57BL/6 mice model.

METHODS: Sixty 3-week-old C57BL/6 mice were randomly divided into experimental groups and normal groups(NC)which totally include four groups: form-deprived 3wk group(FDM3W, n=20), form-deprived 4wk group(FDM4W, n=20), FDM3W normal control group(FDM3W-NC, n=10)and FDM4W normal control group(FDM4W-NC, n=10). Mice in experimental groups were treated with diffuser wearing on right eyes(MD-T), and their left eyes were naturally exposed as their self-control group(MD-C). The normal control groups were free of all the treatments, but the same measurements were performed at the same time-point. Refractive status was examined at 3 and 4wk after treatments in all mice. The histological analysis was applied to assess the changes of the sclera and the retina. The immunohistochemical staining and quantitative real-time PCR(QRT-PCR)were applied to investigate the expression of Smad1 protein and mRNA in retina.

RESULTS:(1)There was no significant difference between right and left eyes in every group before experiment. The normal control eyes showed physiological farsighted development and the MD eyes demonstrated relatively myopization. After experiments, a significant myopia shift had been induced in MD-T compared with MD-C and NC(P<0.05).(2)Histopathologic examination showed posterior sclera and retina in MD-T were thinner than in MD-C and NC groups. Compared with MD-C and NC groups, the expression of Smad1 in retina in MD-T was significantly decreased(P<0.01).

CONCLUSION:The expression of Smad1 in retina of form-deprived myopia was down-regulated, and Smad1 likely to be involved in the development of myopia through the transduction of retinal signal.