Person:

Dang, Quynh

Increased flow resistance is responsible for the elevated intraocular pressure characteristic of glaucoma, but the cause of this resistance increase is not known. We tested the hypothesis that altered biomechanical behavior of Schlemm’s canal (SC) cells contributes to this dysfunction. We used atomic force microscopy, optical magnetic twisting cytometry, and a unique cell perfusion apparatus to examine cultured endothelial cells isolated from the inner wall of SC of healthy and glaucomatous human eyes. Here we establish the existence of a reduced tendency for pore formation in the glaucomatous SC cell—likely accounting for increased outflow resistance—that positively correlates with elevated subcortical cell stiffness, along with an enhanced sensitivity to the mechanical microenvironment including altered expression of several key genes, particularly connective tissue growth factor. Rather than being seen as a simple mechanical barrier to filtration, the endothelium of SC is seen instead as a dynamic material whose response to mechanical strain leads to pore formation and thereby modulates the resistance to aqueous humor outflow. In the glaucomatous eye, this process becomes impaired. Together, these observations support the idea of SC cell stiffness—and its biomechanical effects on pore formation—as a therapeutic target in glaucoma.

AIM: As engineered nanoparticles (ENPs) increasingly enter consumer products, humans become increasingly exposed. The first line of defense against ENPs is the epithelium, the integrity of which can be compromised by wounds induced by trauma, infection, or surgery, but the implications of ENPs on wound healing are poorly understood. MATERIALS & METHODS: Herein, we developed an in vitro assay to assess the impact of ENPs on the wound healing of cells from human cornea. RESULTS & DISCUSSION: We show that industrially relevant ENPs impeded wound healing and cellular migration in a manner dependent on the composition, dose and size of the ENPs as well as cell type. CuO and ZnO ENPs impeded both viability and wound healing for both fibroblasts and epithelial cells. Carboxylated polystyrene ENPs retarded wound healing of corneal fibroblasts without affecting viability. CONCLUSION: Our results highlight the impact of ENPs on cellular wound healing and provide useful tools for studying the physiological impact of ENPs.