Abstract
Background: Outflow regulation and phagocytosis are key functions of the trabecular meshwork (TM), but it is not clear how the two are related in secondary open angle glaucomas characterized by an increased particle load. We hypothesized that diminished TM phagocytosis is not the primary cause of early ocular hypertension and recreated pigment dispersion in a porcine ex vivo model. Methods: Sixteen porcine anterior chamber cultures received a continuous infusion of pigment granules (Pg), while 16 additional anterior chambers served as controls (C). Pressure transducers recorded the intraocular pressure (IOP). The phagocytic capacity of the trabecular meshwork was determined by fluorescent microspheres. Results: The baseline IOPs in Pg and C were similar ( P=0.82). A significant IOP elevation occurred in Pg at 48, 120, and 180 hours (all P<0.01, compared to baseline). The pigment did not cause a reduction in TM phagocytosis at 48 hours when the earliest IOP elevation occurred, but at 120 hours onward ( P=0.001 compared to C). This reduction did not result in an additional IOP increase at 120 or 180 hours compared to the first IOP elevation at 48 hours ( P>0.05). Conclusions: In this porcine model of pigmentary glaucoma, an IOP elevation occurs much earlier than when phagocytosis fails, suggesting that two separate mechanisms might be at work.
Highlights
The conventional outflow is guarded by the trabecular meshwork (TM), a complex three dimensional, layered tissue that contains variable amounts of extracellular matrix (ECM)[1]
We recently developed a porcine ex vivo pigmentary glaucoma (PG) model that recreates the intraocular pressure (IOP) elevation, stress fiber formation, and phagocytosis reduction that are characteristic of human PG8
Pigment granules were seen phagocytosed by trabecular meshwork cells, in the uveal TM, at 48, 120, and 180 hours (Figure 1B, C and D) but were not dense enough to physically obstruct any part of the conventional outflow system
Summary
The conventional outflow is guarded by the trabecular meshwork (TM), a complex three dimensional, layered tissue that contains variable amounts of extracellular matrix (ECM)[1]. A chronic phagocytosis demand in the form of pigment[12], erythrocyte-derived ghost cells[13], inflammatory cells[14], photoreceptor outer segments[15], lens and pseudoexfoliation material[16,17] can all lead to secondary glaucomas even though the amount of material itself is unlikely to cause a physical outflow obstruction. These glaucomas make for a sizable fraction of open angle glaucomas, it was difficult to study the cellular mechanism that leads to an IOP elevation. Conclusions: In this porcine model of pigmentary glaucoma, an IOP elevation occurs much earlier than when phagocytosis fails, suggesting that two separate mechanisms might be at work
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