Abstract
PURPOSE: Secondary open-angle glaucoma may develop as a postoperative complication of early childhood cataract surgery. Its mechanism is poorly understood. Surgical removal of cataracts is typically incomplete, and we estimate that this disease is associated with alpha-B crystallin (CRYAB) secreted from the retained lens material. This study, for the first time, focused on the role of CRYAB in undesired changes of the structures and functions in trabecular meshwork (TM) cells. METHODS: Cell proliferation and migration were assessed using a cell counting kit-8 (CCK8) and transwell assay analysis, respectively. Immunofluorescence (IF), quantitative real-time PCR (Rt-qPCR), and Western blot were performed to determine the effect of CRYAB on F-actin, tight junctions, and the expression of epithelial to mesenchymal transition- (EMT-) associated proteins in TM cells. RESULTS: CRYAB promoted proliferation (p < 0.0001), migration (p < 0.001), and F-actin reorganization in TM cells. There were statistically significant increases in the mRNA and protein levels of zo-1, cadherin-N, and vimentin (all p < 0.0001) and cadherin-E decreased (p < 0.0001) and the mRNA level of claudin-1 increased (p < 0.0001) compared to those of the control group. CONCLUSION: All of the changes in structures and functions first observed in the TM cells after exposure to CRYAB resembled alterations seen in primary open-angle glaucoma, suggesting that CRYAB might be related to the pathogenesis of secondary open-angle glaucoma after congenital cataract surgery.