SPARC-null mice have lower IOPs than do their WT counterparts with equal CCTs. The rate of aqueous turnover suggests that the mechanism is enhanced outflow resistance.

PURPOSE. Thrombospondin-1 (TSP1) and TSP2 are matricellular proteins that have been shown to regulate cytoskeleton, cell adhesion, and extracellular matrix remodeling. Both TSP1 and TSP2 are found in the trabecular meshwork (TM). In cadaver eyes with primary open-angle glaucoma (POAG), TSP1 is increased in one third of patients. We hypothesized that TSP1 and TSP2 participate in the regulation of intraocular pressure (IOP).METHODS. IOPs of TSP1-null, TSP2-null mice, and their corresponding wild-type (WT) mice were measured using a commercial rebound tonometer. Fluorophotometric measurements assessed aqueous turnover. Central corneal thickness (CCT) was measured by optical coherence tomography. Iridocorneal angles were examined using light microscopy (LM), immunofluorescence (IF), and transmission electron microscopy (TEM).RESULTS. Average IOPs of TSP1-null and TSP2-null mice were 10% and 7% less than that of the corresponding WT mice, respectively. CCTs were 6.5% less in TSP1-null mice (P < 0.05) and 1.1% less in TSP2-null mice (P > 0.05). Fluorophotometric measurements suggest that aqueous turnover rates in TSP1-null and TSP2-null mice are greater than those of WT mice. LM of the TSP1-null and TSP2-null iridocorneal angles reveals morphology, which is indistinguishable from that of their corresponding WTs. IF revealed possible concurrent underexpression of TSP2 in TSP1-null mice and of TSP1 in TSP2-null mice. TEM revealed larger collagen fibril diameters in TSP1-null and TSP2-null mice compared with WTs.CONCLUSIONS. TSP1-null and TSP2-null mice have lower IOPs than their WT counterparts. The rate of aqueous turnover suggests that the mechanism is enhanced outflow facility. An alteration in the extracellular matrix may contribute to this finding. (Invest Ophthalmol Vis Sci. 2012;53:6708-6717)

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Glaucoma is the leading cause of irreversible vision loss post-keratoplasty and an important cause of graft failure. With newer techniques, such as lamellar, endothelial, and laser-assisted keratoplasty as well as keratoprosthesis gaining popularity, clinicians will need to consider the incidence, risks, evaluation, and management of glaucoma for each type of keratoplasty when determining which type of transplant may be most appropriate. A comprehensive literature search of glaucoma in the setting of corneal transplantation was performed and serves as the basis for this review. Preexisting glaucoma and aphakia are notable risk factors. Patients that are candidates for deep anterior lamellar keratoplasty may benefit from reduced rates of post-keratoplasty glaucoma. Although glaucoma also complicates eyes with Descemet stripping endothelial keratoplasty, the severity is less and the intraocular pressure is more easily controlled when compared to penetrating keratoplasty. Endothelial keratoplasty creates unique perioperative issues mostly related to management of anterior chamber air bubbles.

Elimination of LOXL1 in mice impairs the blood-aqueous humor barrier in the ocular anterior segment and causes lens abnormalities consistent with cataract formation, but does not result in deposition of macromolecular material or glaucoma. These results show that mice lacking LOXL1 have some ES features but that complete disease manifestation requires other factors that could be genetic and/or environmental.

TNC does not appear to contribute directly to outflow resistance. However, TNC immunolocalization in the JCT of adult human eyes suggests that certain areas of the TM are being continuously remodeled with or without an IOP increase.

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