Mutations in the gene optineurin (OPTN) have been associated with primary-open angle glaucoma. Here we present a study on the level of OPTN gene expression in the human trabecular meshwork in response to increased perfusion pressure in the anterior chamber perfusion model of the human eye. Perfusion pressure was raised from 10 to 30 mm Hg for periods ranging between 1 and 24 h. OPTN transcript levels in the trabecular meshwork were determined using real-time quantitative polymerase chain reaction. The results show no statistically significant alteration of the OPTN transcript level after raising the pressure. Moreover, no changes were detected in the transcript levels of the 3 known OPTN isoforms. This result shows that enhanced pressure levels do not lead to rapid changes in gene expression levels of OPTN in human trabecular meshwork. This suggests that alterations in OPTN gene expression are not involved in the mechanisms regulating aqueous humor outflow after an increase in intraocular eye pressure.

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