Zinc oxide nanoparticles ameliorate collagen lattice contraction in human tenon fibroblasts.

Glaucoma is a major cause of irreversible blindness in the world and filtering surgery is commonly carried out to control intraocular pressure. Failure of filtering surgery is usually due to postoperative scarring, and fibroblast proliferation, collagen production and subconjunctival fibrosis play a prominent role in obstructing aqueous humor from the anterior chamber to the subconjunctival space. Zinc oxide (ZnO) nanoparticles have been widely applied in biomedical fields. However, the influence of ZnO nanoparticles on human tenon fibroblasts (HTFs) is still unclear. In the present study, we first explored the effects of various concentrations of ZnO nanoparticles on HTFs proliferation, reactive oxygen species (ROS) generation, cell cycle arrest, and apoptosis. Further, we determined the changes of transforming growth factor-β (TGF-β1), fibronectin (FN) extra domain A (ED-A), and procollagen I carboxyterminal propeptide (PICP) at mRNA and protein levels, explored the effect of ZnO nanoparticles on the collagen lattice contraction in HTFs. The results indicated that ZnO nanoparticles can efficiently inhibit HTFs proliferation, elevate ROS production level, and induce cell cycle arrest at G2/M phase, leading to HTFs apoptosis. ZnO nanoparticles can also decrease the expressions of TGF-β1, ED-A, and PICP at mRNA and protein levels; significantly prevent fibroblast-mediated collagen lattice contraction. Taken together, ZnO nanoparticles can efficiently ameliorate collagen lattice contraction in HTFs, and may be a promising antifibrotic agent in glaucoma filtration surgery. Our findings provide a new insight on anti-scar formation after glaucoma filtration surgery by using ZnO nanoparticles.